Manual of Cardiology
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4.17-Kronzon-M-Mode-Echo.Pdf
M-Mode Echocardiography Is it still Alive? Itzhak Kronzon, MD,FASE Honoraria: Philips Classical M-mode Echocardiography M-Mode offers better time and image resolution. Sampling Rate M-Mode: 1800 / sec 2D: 30 / sec Disadvantages 1. Single Dimension (depth only) 2. Nonperpendicular orientation (always use 2D guidance). Normal MV MS M-Mode of RA & LA Myxomas Back cover of ECHOCARDIOGRAPHY Feigenbaum, 3rd edition MV Prolapse M-Mode in HOCM ASH / SAM Mid-systolic AV Closure Markers of LV Dysfunction A-C Shoulder (“B-Bump”) EPSS Feigenbaum, ECHOCARDIOGRAPHY What does the m-mode show? 1. MS 2. AI 3. Flail MV 4. Myxoma Answer: 3. Posterior Leaflet Motion in Flail MV Note that the posterior leaflet moves anteriorly in early diastole, before it moves posteriorly. ASD with Large L to R Shunt Note markedly dilated RV and “paradoxical” septal motion Dyssynchrony by M-Mode -LBBB 138msec Dyssynchrony of >130msec is associated with good CRT response (sensitivity 100%, specificity 63%) This M mode finding is not associated with increased risk of A. Coarctation B. Pulmonic Stenosis C. Subaortic Stenosis D. Aortic insufficiency Echo of pt with Endocarditis and Shock Best Rx is: 1. AVR 2. MVR 3. IABP 4. Can not tell Echo of pt with Endocarditis and Shock Answer: 1. AVR Note premature closure of MV & echogenic mass in LVOT (Ao veg. Vs. flail Ao cusp) Differential Dx of Premature MV Closure A. AR B. First Degree AV Block C. High Degree AV Block D. Blocked APC E. Atrial Flutter The most likely physical finding in this pt is 1. Absent left subclavian pulse 2. -
Rheumatic Heart Disease in Children: from Clinical Assessment to Therapeutical Management
European Review for Medical and Pharmacological Sciences 2006; 10: 107-110 Rheumatic heart disease in children: from clinical assessment to therapeutical management G. DE ROSA, M. PARDEO, A. STABILE*, D. RIGANTE* Section of Pediatric Cardiology, *Department of Pediatric Sciences, Catholic University “Sacro Cuore” – Rome (Italy) Abstract. – Rheumatic heart disease is presence of valve disease or carditis can be still a relevant problem in children, adolescents easily recognized through echocardiographic and young adults. Molecular mimicry between examinations, but the combination of clinical streptococcal and human proteins has been pro- posed as the triggering factor leading to autoim- tools and echocardiography consents the munity and tissue damage in rheumatic heart most accurate assessment of heart involve- disease. Despite the widespread application of ment2. It is well known however that minimal Jones’ criteria, carditis is either underdiagnosed physiological mitral regurgitation can be or overdiagnosed. Endocarditis leading to mitral identified in normal people and might over- and/or aortic regurgitation influences morbidity diagnose the possibility of carditis. Only in and mortality of rheumatic heart disease, whilst myocarditis and pericarditis are less significant 30% patients serial electrocardiogram studies in determining adverse outcomes in the long- are helpful in the diagnosis of acute RF with term. Strategy available for disease control re- non-specific findings including prolonged PR mains mainly secondary prophylaxis with the interval, atrio-ventricular block, diffuse ST-T long-acting penicillin G-benzathine. changes with widening of the QRS-T angle and inversion of T waves. Carditis as an ini- Key Words: tial sign might be mild or even remain unrec- Rheumatic heart disease, Pediatrics. -
Case Reports
Case Reports Quadrivalvular Heart Disease An Autopsied Case with Massive Pulmonary Regurgitation Tsuguya SAKAMOTO, M.D., Zen'ichiro UOZUMI, M.D., Nobuyoshi KAWAI, M.D., Yoshiyuki SAKAMOTO, M.D., Ryoko KATO, M.D., and Hideo UEDA, M.D. SUMMARY An autopsied case of quadrivalvular heart disease was described, in which pulmonary regurgitation due to possible bicuspid valve was pre- dominant and tricuspid stenosis, mitral stenosis, and aortic stenosis with insufficiency coexisted. The patient was 47, and finally 53 years old female with long-term history of cough due to bronchial compression by the enormously dilated pulmonary artery. Clinical examination revealed massive pulmonary regurgitation, which was further substantiated by right heart catheterization and cineangiocardiography. The phono- cardiograms and the reference tracings suggested the co-existence of tricuspid stenosis, aortic stenosis with regurgitation and mitral stenosis. Cardiac catheterization, intracardiac phonocardiography and angio- cardiography also favored to the diagnosis of organic tricuspid stenosis. However, the ignorance of the presence of such an unusual combination misled to the precise antemortem diagnosis. Discussion was made on the rarity of quadrivalvular heart disease, and the pathogenesis of this unusual pulmonary regurgitation was analyzed based on the autopsy finding and the history as well as the clinical mani- festation. Finally, combination of the murmurs of organic and relative tricuspid stenosis was presented to explain the acoustical findings of the present case. Additional Indexing Words: Phonocardiography Mechanocardiography Bronchial compression Right-sided Austin Flint murmur UADRIVALVULAR heart disease was first described by Shattuck1) in 1891. However, the involvement of all four valves in a given patient is extremely rare.2) The present paper describes one of such case, in which From the Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Tokyo. -
CARDIOLOGY Section Editors: Dr
2 CARDIOLOGY Section Editors: Dr. Mustafa Toma and Dr. Jason Andrade Aortic Dissection DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY (CONT’D) CARDIAC DEBAKEY—I ¼ ascending and at least aortic arch, MYOCARDIAL—myocardial infarction, angina II ¼ ascending only, III ¼ originates in descending VALVULAR—aortic stenosis, aortic regurgitation and extends proximally or distally PERICARDIAL—pericarditis RISK FACTORS VASCULAR—aortic dissection COMMON—hypertension, age, male RESPIRATORY VASCULITIS—Takayasu arteritis, giant cell arteritis, PARENCHYMAL—pneumonia, cancer rheumatoid arthritis, syphilitic aortitis PLEURAL—pneumothorax, pneumomediasti- COLLAGEN DISORDERS—Marfan syndrome, Ehlers– num, pleural effusion, pleuritis Danlos syndrome, cystic medial necrosis VASCULAR—pulmonary embolism, pulmonary VALVULAR—bicuspid aortic valve, aortic coarcta- hypertension tion, Turner syndrome, aortic valve replacement GI—esophagitis, esophageal cancer, GERD, peptic OTHERS—cocaine, trauma ulcer disease, Boerhaave’s, cholecystitis, pancreatitis CLINICAL FEATURES OTHERS—musculoskeletal, shingles, anxiety RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC PATHOPHYSIOLOGY AORTIC DISSECTION? ANATOMY—layers of aorta include intima, media, LR+ LRÀ and adventitia. Majority of tears found in ascending History aorta right lateral wall where the greatest shear force Hypertension 1.6 0.5 upon the artery wall is produced Sudden chest pain 1.6 0.3 AORTIC TEAR AND EXTENSION—aortic tear may Tearing or ripping pain 1.2–10.8 0.4–0.99 produce -
Cardiology 2
Ch02.qxd 7/5/04 3:06 PM Page 13 Cardiology 2 FETAL CARDIOVASCULAR PHYSIOLOGY The ‘basic science’ nature of this topic – as well as the potential pathological implications in paediatric cardiology – makes it a likely viva question. Oxygenated blood from the placenta returns to the fetus via the umbilical vein (of which there is only one). Fifty per cent traverses the liver and the remaining 50% bypasses the liver via the ductus venosus into the inferior vena cava. In the right atrium blood arriving from the upper body from the superior vena cava (low oxygen saturation) preferentially crosses the tricus- pid valve into the right ventricle and then via the ductus flows into the descending aorta and back to the placenta via the umbilical arteries (two) to reoxygenate. The relatively oxygenated blood from the inferior vena cava, however, preferentially crosses the foramen ovale into the left atrium and left ventricle to be distributed to the upper body (including the brain and coro- nary circulation). Because of this pattern of flow in the right atrium we have highly oxygenated blood reaching the brain and deoxygenated blood reach- ing the placenta. High pulmonary arteriolar pressure ensures that most blood traverses the pulmonary artery via the ductus. Changes at birth 1. Occlusion of the umbilical cord removes the low-resistance capillary bed from the circulation. 2. Breathing results in a marked decrease in pulmonary vascular resistance. 3. In consequence, there is increased pulmonary blood flow returning to the left atrium causing the foramen ovale to close. 4. Well-oxygenated blood from the lungs and the loss of endogenous prostaglandins from the placenta result in closure of the ductus arteriosus. -
Cardiology 1
Cardiology 1 SINGLE BEST ANSWER (SBA) a. Sick sinus syndrome b. First-degree AV block QUESTIONS c. Mobitz type 1 block d. Mobitz type 2 block 1. A 19-year-old university rower presents for the pre- e. Complete heart block Oxford–Cambridge boat race medical evaluation. He is healthy and has no significant medical history. 5. A 28-year-old man with no past medical history However, his brother died suddenly during football and not on medications presents to the emergency practice at age 15. Which one of the following is the department with palpitations for several hours and most likely cause of the brother’s death? was found to have supraventricular tachycardia. a. Aortic stenosis Carotid massage was attempted without success. b. Congenital long QT syndrome What is the treatment of choice to stop the attack? c. Congenital short QT syndrome a. Intravenous (IV) lignocaine d. Hypertrophic cardiomyopathy (HCM) b. IV digoxin e. Wolff–Parkinson–White syndrome c. IV amiodarone d. IV adenosine 2. A 65-year-old man presents to the heart failure e. IV quinidine outpatient clinic with increased shortness of breath and swollen ankles. On examination his pulse was 6. A 75-year-old cigarette smoker with known ischaemic 100 beats/min, blood pressure 100/60 mmHg heart disease and a history of cardiac failure presents and jugular venous pressure (JVP) 10 cm water. + to the emergency department with a 6-hour history of The patient currently takes furosemide 40 mg BD, increasing dyspnoea. His ECG shows a narrow complex spironolactone 12.5 mg, bisoprolol 2.5 mg OD and regular tachycardia with a rate of 160 beats/min. -
The Austin Flint Murmur Phonocardiographic and Patho
The Austin Flint Murmur Phonocardiographic and Patho-anatomical Study Hideo UEDA, M. D., Tsuguya SAKAMOTO, M. D., Nobuyoshi KAWAI, M. D., Hiroshi WATANABE, M. D., Zen'ichiro UozuMI, M. D., Ryozo OKADA, M. D., Tohru KOBAYASHI, M. D., Tetsuro YAMADA, M. D., Kiyoshi INOUE, M. D., and Goro KAITO, M. D. Clinical, phonocardiographic and patho-anatomical studies were made on 15 cases with the Austin Flint murmur. The phonocardio- graphic characteristics were pointed out, and the mode of production of this murmur was explained based on the patho-anatomy of the mitral valve. Several typical cases were illustrated. INCE the last century, the Austin Flint murmur, a well-known apical diastolic rumble in aortic insufficiency,1) has been extensively debated by many authors. 2)-49) However, despite the ample arguments on the incidence, acoustic and graphic characteristics, clinical background and cardiac patho- logy, a comprehensive study with the phonocardiographic as well as patho- logic confirmation has not been attempted up to the present time. The purpose of the present study is, therefore, to investigate these figures based on the clinico-pathological observations. Particular attention was paid to search for the auscultatory and phonocardiographic characteristics of the Austin Flint murmur, and to observe whether any patho-anatomical factors seem to be responsible for the production of this murmur. MATERIAL AND METHOD Out of the autopsy cases from the Second Department of Internal Medicine, Tokyo University Hospital, 14 cases of •gisolated•h aortic insufficiency had com- plete clinical examination including phonocardiography. The cases with con- comitant •gorganic•h mitral insufficiency were not included in this series. -
Rheumatic Heart Disease
RHEUMATIC HEART DISEASE Rheumatic fever is an acute immunologically mediated multisystem inflammatory disease that occurs few weeks after an attack of group A beta- hemolytic streptococcal pharyngitis. It is not an infective disease. The most commonly affected age group is children between the ages of 5-15 yearsQ. The disease is a type II hypersensitivity reaction in which antibodies against ‘M’ protein of some streptococcal strains (1, 3, 5, 6, and 18) cross-react with the glycoprotein antigens in the heart, joints and other tissues (molecular mimicry). CLINICAL FEATURES It presents with fever, anorexia, lethargy and joint pain 2-3 WEEKS after an episode of Streptococcal Infection is required for diagnosis Migratory Polyarthritis is the commonest major manifestation. Q Salient feature`s of the major criteria Carditis All the layers of the heart namely pericardium, myocardium and endocardium are involved, so this is called pancarditis. The pericarditis is associated with fibrinous/serofibrinous exudate and is called as ‘bread and butter’ pericarditis. It may manifest as breathlessness (due to heart failure or pericardial effusion), palpitations or chest pain (usually due to pericarditis or pancarditis). Other features include tachycardia, cardiac enlargement and new or changed murmurs. A soft mid-diastolic murmur (the Carey Coombs murmur) is typically due to valvulitis, with nodules forming on the mitral valve leaflets. Aortic regurgitation occurs in 50% of cases but the tricuspid and pulmonary valves are rarely involved. Pericarditis may cause chest pain, a pericardial friction rub and precordial tenderness. Cardiac failure may be due to myocardial dysfunction or valvular regurgitation. Valvular involvement is common in rheumatic heart disease. -
Ministry of Health of Ukraine Kharkiv National Medical University
Ministry of Health of Ukraine Kharkiv National Medical University AUSCULTATION OF THE HEART. NORMAL HEART SOUNDS, REDUPLICATION OF THE SOUNDS, ADDITIONAL SOUNDS (TRIPLE RHYTHM, GALLOP RHYTHM), ORGANIC AND FUNCTIONAL HEART MURMURS Methodical instructions for students Рекомендовано Ученым советом ХНМУ Протокол №__от_______2017 г. Kharkiv KhNMU 2017 Auscultation of the heart. normal heart sounds, reduplication of the sounds, additional sounds (triple rhythm, gallop rhythm), organic and functional heart murmurs / Authors: Т.V. Ashcheulova, O.M. Kovalyova, O.V. Honchar. – Kharkiv: KhNMU, 2017. – 20 с. Authors: Т.V. Ashcheulova O.M. Kovalyova O.V. Honchar AUSCULTATION OF THE HEART To understand the underlying mechanisms contributing to the cardiac tones formation, it is necessary to remember the sequence of myocardial and valvular action during the cardiac cycle. During ventricular systole: 1. Asynchronous contraction, when separate areas of myocardial wall start to contract and intraventricular pressure rises. 2. Isometric contraction, when the main part of the ventricular myocardium contracts, atrioventricular valves close, and intraventricular pressure significantly increases. 3. The ejection phase, when the intraventricular pressure reaches the pressure in the main vessels, and the semilunar valves open. During diastole (ventricular relaxation): 1. Closure of semilunar valves. 2. Isometric relaxation – initial relaxation of ventricular myocardium, with atrioventricular and semilunar valves closed, until the pressure in the ventricles becomes lower than in the atria. 3. Phases of fast and slow ventricular filling - atrioventricular valves open and blood flows from the atria to the ventricles. 4. Atrial systole, after which cardiac cycle repeats again. The noise produced By a working heart is called heart sounds. In auscultation two sounds can be well heard in healthy subjects: the first sound (S1), which is produced during systole, and the second sound (S2), which occurs during diastole. -
Cardiovascular Pathology the Perfect Preparation for USMLE® Step 1
Cardiovascular Pathology The Perfect Preparation for USMLE® Step 1 2021 Edition You cannot separate passion from pathology any more than you can separate a person‘s spirit from his body. (Richard Selzer) www.lecturio.com Cardiovascular Pathology eBook Live as if you were to die tomorrow. Learn as if you were to live forever. (Mahatma Gandhi) Pathology is one of the most-tested subjects on the USMLE® Step 1 exam. At the heart of the pathology questions on the USMLE® exam is cardiovascular pathology. The challenge of cardiovascular pathology is that it requires students to be able to not only recall memorized facts about cardiovascular pathology, but also to thoroughly un- derstand the intricate interplay between cardiovascular physiology and pathology. Understanding cardiovascular pathology will not only allow you to do well on the USMLE® Step 1 exam, but it will also serve as the foundation of your future patient care. This eBook... ✓ ...will provide you with everything you need to know about cardiovascular pathology for your USMLE® Step 1 exam. ✓ ...will equip you with knowledge about the most important diseases related to the cardiovascular system, as well as build bridges to the related medical sciences, thus providing you with the deepest understanding of all cardiovascular pathology topics. ✓ ...is specifically for students who already have a strong foundation in the basic sciences, such as anatomy, physiology, biochemistry, microbiology & immunology, and pharmacology. Elements of this eBook High-yield: Murmurs of grade III and above are High-yield-information will help you to focus on the most important facts. usually pathological. (...) A number of descriptive pictures, mnemonics, and overviews, but also a reduction to the essentials, will help you to get the best out of your learning time. -
Dynamic Auscultation
TOP 10 TAKEAWAYS… Jane A. Linderbaum MS, APRN, CNP, AACC Assistant Professor of Medicine Department of cardiovascular disease No Disclosures No off-label discussions 73% of survey respondents identified a need for improved knowledge of CV pathophysiology #10 CARDIAC CIRCULATION, KNOW IT AND LOVE IT The Cardiac Cycle The heart sounds • S1 Mitral (and tricuspid) valve closure Soft if poor EF, loud if good EF • S2 Aortic and pulmonary valve closure Loud if aortic (pulm) pressure • S3 – means “restrictive” filling • S4 – means “abnormal” filling Listening Posts for Auscultation AV – 2nd RICS PV – 2nd LICS MV – 5-6th LICS @ the apex TV – 5-6th LICS parasternal 83% of survey respondents identified themselves as early career in clinic/hospital consult practices # 9 COMMON SYSTOLIC MURMURS YOU WILL DIAGNOSE AND MANAGE MITRAL REGURGITATION MR Treatment • Treat underlying conditions • Consider MV repair when possible at experienced center • Consider MV replacement before ventricle dilates and/or function decreases MITRAL VALVE PROLAPSE Mitral Valve Prolapse Pearls • CHANGE in Murmur (from click-murmur or isolated late sys murmur to holosystolic without audible click) • Skeletal deformities in up to 50% • Upright posture enhances auscultation of the mid-late systolic murmur • May develop severe MR, refer for additional testing as patient may be candidate for mitral valve repair • Murmur may INCREASE with Valsalva • Typically do not require SBE prophylaxis Hypertrophic Cardiomyopathy Hypertrophic Cardiomyopathy • Vigorous LV apical impulse – sustained -
Valvular Heart Disease Systolic Murmurs (ASMR) Diastolic Murmurs (MSAR) Aortic Stenosis (AS) Mitral Regurg
Valvular heart disease Systolic murmurs (ASMR) Diastolic murmurs (MSAR) Aortic stenosis (AS) Mitral regurg. (MR) Mitral stenosis (MS) Aortic regurg. (AR) Causes 1-Calcification and degeneration of 1-Rheumatic heart disease 1- Rheumatic Fever; 1-Rheumatic heart disease a normal valve (elderly) 2- MVP (prolapse) 2- Other less common 2-Aortic aneurysm \ Dissection. 2-Calcification and fibrosis of a 3- Endocarditis causes: 3-Inflammation congenitally bicuspid aortic valve 4- Ischemic heart disease Congenital Mitral Stenosis, SLE, 4-Degeneration 3-Rheumatic valvular disease 5- Myocarditis Rheumatoid Arthritis, Atrial 5- Severe Hypertension 6- Cardiomyopathies Myxoma (tumor), Malignant 6-Bicuspid aortic valve 7- Myxomatus degenration Carcinoid, Bacterial Endocarditis 7-Endocarditis 8- Marfan's syndrome Pathophysiology 1.Obstructed LV emptying 1. increased LA pressure and 1.LA hypertension: - Stroke volume increased (high (pressure overload) decreased forward CO and - Pulmonary interstitial edema. Systolic BP) 2. Left ventricular hypertrophy Afterload. - Pulmonary hypertension - Regurgitant volume increased 3. ↑LV diastolic pressure: 2. Volume overload occurs, - Leads to right heart failure / CHF (Low Diastolic BP) → Pulmonary - ↑ LA pressure → pulmonary increasing preload. - LA stretch & atrial fibrillation venous congestion venous congestion 2. Limited LV filling & cardiac - ↓ perfusion pressure. output. symptoms - Angina (imbalance - Fatigue & weakness - Malar flush - Dyspnea on exertion (most between supply & demand) - Dyspnea - Dyspnea on exertion common complaint) - Syncope with exertion - Orthopnea, PND - Fatigue - Fatigue. - Dyspnea - Right sided HF (in the late - Orthopnea, PND, - Diminished exercise - Congestive heart failure stages of the disease) & - Palpitation, Chest pain, tolerance. (CHF) eventually may lead to Peripheral edema. - Angina (Imbalance CHF. - Hoarseness between myocardial supply - Systemic embolism & demand) - Hemoptysis (10%) Signs - Pulsus Parvus et Tardus - Systolic thrill.