DOCSLIB.ORG

Additional Heart Sounds–Part 2 (Clicks, Opening Snap and More)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Additional Heart Sounds–Part 2 (Clicks, Opening Snap and More) Published online: 2020-12-23 THIEME Clinical Rounds 351 Additional Heart Sounds–Part 2 (Clicks, Opening Snap and More) Lalita Nemani1 Ramya Pechetty2 1Department of Cardiology, Nizam’s Institute of Medical Sciences, Address for correspondence Lalita Nemani, MD, DM, Department Hyderabad, Telangana, India of Cardiology, Nizam’s Institute of Medical Sciences, Hyderabad, 2Department of Cardiology, Apollo Hospitals, Jubilee Hills, Telangana, India (e-mail: [email protected]). Hyderabad, Telangana, India Ind J Car Dis Wom:2020;5:351–363 Abstract Systolic clicks are high-pitched sharp sounds. They are classified as ejection and none- jection clicks. Ejections clicks commonly occur at the aortic and pulmonary valve, while nonejection clicks occur at the mitral and tricuspid valve. Keywords Opening snap is an additional sound heard in the diastole. It is described as an early ► ejection click diastolic, high-pitched sound, which is associated with opening of the mitral and/or ► nonejection clicks tricuspid valve. ► mitral valve prolapse Pericardial knock is a high-pitched early diastolic sound, which is characteristic of con- ► opening snap strictive pericarditis. ► pericardial friction rub The opening and closing of prosthetic valves produce sounds which may vary in inten- ► Hammam's crunch sity and timing according to the type and design of the valve, patient’s rhythm, and ► prosthetic sounds hemodynamic status. Systolic Clicks ECs occur at the maximal opening of the semilunar valves. Being high frequency sounds, they are best heard 1-4 Systolic clicks are high-pitched sharp sounds. They are with the diaphragm. ECs result from opening of the ste- classified as ejection and nonejection clicks. Ejections clicks notic/diseased aortic and pulmonary valves or from normal (ECs) commonly occur at the aortic and pulmonary valve, valves in the presence of dilated aorta or pulmonary artery. while non-ejection clicks occur at the mitral and tricuspid Types of ECs: ECs are classified as valvular or vascular. valve ( ). ►Fig. 1 Valvular clicks: They result from abnormal aortic and pul- Technique of auscultation and detection of systolic click: monary valves. Clicks are best heard with the diaphragm of the stethoscope Mechanism: Abrupt opening of aortic and pulmonary and are loudest at their respective auscultatory areas (►Fig. 2). valves generate ECs. The abrupt halting movement of the dis- They are identified as sharp additional sound in the sys- eased valves produces this audible sound (►Fig. 4). tole by simultaneous auscultation of the heart and carotid artery palpation to rightly identify S1 and S2. They are fur- A. Aortic valvular click. ther identified as early, mid, and late systolic clicks and eval- a. Valvular aortic stenosis (AS). uated in relation to dynamic maneuvers. b. Congenital bicuspid aortic valve. c. Congenital quadricuspid aortic valve as in truncus Ejection Clicks (ECs) arteriosus. They are sharp high-pitched sounds heard in early systole B. Pulmonary valvular click. just after the first heart sound (►Fig. 3). a. Valvular pulmonary stenosis. published online DOI https://doi.org/ ©2020. Women in Cardiology and Related Sciences. December 23, 2020 10.1055/s-0040-1722385. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/). Thieme Medical and Scientific Publishers Pvt. Ltd. A-12, 2nd Floor, Sector 2, Noida-201301 UP, India 352 Additional Heart Sounds Nemani and Pechetty Fig. 4 Mechanism of valvular ejection click. Fig. 1 Classification of systolic clicks. Fig. 5 Effect of respiration on pulmonary and aortic valvular click. Table 1. Clinical characteristics of aortic and pulmonary valvular click Aortic valvular Pulmonary valvular click click Site of best Widely heard Localized audibility Best heard at the Best heard in the second apex followed by left intercostal space Fig. 2 Auscultation sites on precordium. right second inter- coastal space Respiration Not affected Decrease in intensity and (Fig. 5) occurs early/ merge with S1 in inspiration Carotid Immediately before Usually before or with the upstroke or coincident initial carotid upstroke, with initial carotid however a delay in onset upstroke favors pulmonary origin Relation Occurs 120 to 140 Occurs 90 to 110 millisec- with Q milliseconds after onds after onset of Q wave wave on onset of Q wave on on ECG ECG ECG This notch apparently results from maximal opening Fig. 3 Systolic ejection click. and abrupt deceleration of the flexibly stenotic aortic valve. Clinical characteristics of aortic and pulmonary valvular • Intensity of the sound decreases with calcification. Seen clicks are mentioned below (►Table 1). only with pliable valves and is absent in severe calcific AS. • Calcification of the aortic valve is a rule beyond the age of Clinical Significance 40 years. Hence, presence of aortic ejection click in adults suggests either mild AS or presence of congenital bicuspid 5,6 Ejection Click of Aortic Stenosis (AS) aortic valve. • Diagnostic of valvular AS and is absent in supravalvular or • Presence of an aortic EC in the child is diagnostic of subvalvular AS. congenital bicuspid aortic valve. • It corresponds to the notch in the upstroke of the aortic • Absence of other signs of AS in the presence of aortic EC pressure tracing or the carotid pulse tracing (►Fig. 6). strongly suggests the presence of bicuspid aortic valve. Indian Journal of Cardiovascular Disease in Women WINCARS Vol. 5 No. 4/2020 © 2020 Women in Cardiology and Related Sciences. Additional Heart Sounds Nemani and Pechetty 353 Ejection Click (EC) of Pulmonary Stenosis (PS) 7,8 The S1–pulmonary EC interval is directly related to RV • Diagnostic of valvular PS. isovolumic contraction time. With increasing severity of PS, • It is the only right-sided acoustic event that softens the isovolumic systolic interval shortens resulting in early (diminishes) with inspiration. onset of EC. • Mechanism of inspiratory decrease in the pulmonary EC. • Mild-to-moderate PS–EC becomes soft and occurs earlier. • Severe PS–the RV may become so stiff that a vigorous ◦ In PS, the right ventricle (RV) is stiff and hypertrophied. atrial contraction opens the pulmonary valve completely, ◦ During inspiration, when more blood enters the RV, it producing a click in late diastole. fails to distend normally. As a result, the RV pressure • Very severe PS–the EC fuses with S1 and may not be increases, and exceeds that of the pulmonary artery identified pressure, which falls slightly. The pulmonary valve is partially open (domed or tensed position) prior to Vascular clicks9: They occur in the presence of normal onset of ventricular contraction (►Fig. 7a). When the aortic and pulmonary valves. They result from rapid disten- RV contracts, excursion of the partially opened pul- sion of the dilated proximal aorta or pulmonary artery at the monary valve is reduced and therefore the EC is softer onset of ejection. and occurs earlier. Mechanism: Vascular clicks result from increased pressure, ◦ During expiration, venous return to the right heart is increased flow, and dilatation of the great vessels (►Fig. 8). decreased. At the same time, the pulmonary artery Causes: pressure also rises slightly. As the pulmonary artery A. Aortic vascular click. end-diastolic pressure exceeds the RV pressure, the pulmonary valve leaflets are in a closed or slack posi- a. Systemic hypertension. tion (►Fig. 7b). With ventricular systole, the valve b. Aneurysm of the ascending aorta. opens quickly and then abruptly halts, producing the c. Aortic regurgitation. ejection sound. d. Tetralogy of Fallot–anterior dilated aorta. e. Anemia and thyrotoxicosis–hyperkinetic circulatory states. B. Pulmonary vascular click. a. Pulmonary hypertension. b. Idiopathic dilatation of the pulmonary artery. c. Left-to-right shunts.10 d. Hyperkinetic circulatory states. Clinical characteristics of vascular and valvular clicks11 are shown in ►Table 2. Aortic vascular and valvular clicks can be identified, based on associated clinical features (►Table 3). Pulmonary clicks can be differentiated, based on respira- tory variation and associated clinical features (►Table 4). Fig. 6 Physiological basis of ejection click in aortic stenosis. Significance Aortic vascular click is associated with aortic root dilation in the form of aortic sclerosis with tortuous aortic root, sys- temic hypertension, ascending aortic aneurysm and aortic regurgitation due to aortic root pathology. Fig. 7 (a and b) Respiratory variation of pulmonary ejection click. Fig. 8 Mechanism of vascular clicks. Indian Journal of Cardiovascular Disease in Women WINCARS Vol. 5 No. 4/2020 © 2020 Women in Cardiology and Related Sciences. 354 Additional Heart Sounds Nemani and Pechetty Table 2. Clinical characteristics of vascular and valvular clicks Table 5. S1–EC versus split S1 Vascular clicks Valvular clicks S1–EC Split S1 S2 intensity Loud Normal or Quality of Both are high-pitched Second sound (tricus- diminished sounds sounds pid sound) is a low- pitch sound Split S2 Normal/close/ Wide/reverse single Site of Best heard at the Best heard at the lower audibility base of the heart and sternal border Palpable artery Palpable impalpable apex beyond valve Respiration No variation in case Tricuspid
Load more

Recommended publications
  • Guidelines on the Diagnosis and Management of Pericardial
    European Heart Journal (2004) Ã, 1–28 ESC Guidelines Guidelines on the Diagnosis and Management of Pericardial Diseases Full Text The Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology Task Force members, Bernhard Maisch, Chairperson* (Germany), Petar M. Seferovic (Serbia and Montenegro), Arsen D. Ristic (Serbia and Montenegro), Raimund Erbel (Germany), Reiner Rienmuller€ (Austria), Yehuda Adler (Israel), Witold Z. Tomkowski (Poland), Gaetano Thiene (Italy), Magdi H. Yacoub (UK) ESC Committee for Practice Guidelines (CPG), Silvia G. Priori (Chairperson) (Italy), Maria Angeles Alonso Garcia (Spain), Jean-Jacques Blanc (France), Andrzej Budaj (Poland), Martin Cowie (UK), Veronica Dean (France), Jaap Deckers (The Netherlands), Enrique Fernandez Burgos (Spain), John Lekakis (Greece), Bertil Lindahl (Sweden), Gianfranco Mazzotta (Italy), Joa~o Morais (Portugal), Ali Oto (Turkey), Otto A. Smiseth (Norway) Document Reviewers, Gianfranco Mazzotta, CPG Review Coordinator (Italy), Jean Acar (France), Eloisa Arbustini (Italy), Anton E. Becker (The Netherlands), Giacomo Chiaranda (Italy), Yonathan Hasin (Israel), Rolf Jenni (Switzerland), Werner Klein (Austria), Irene Lang (Austria), Thomas F. Luscher€ (Switzerland), Fausto J. Pinto (Portugal), Ralph Shabetai (USA), Maarten L. Simoons (The Netherlands), Jordi Soler Soler (Spain), David H. Spodick (USA) Table of contents Constrictive pericarditis . 9 Pericardial cysts . 13 Preamble . 2 Specific forms of pericarditis . 13 Introduction. 2 Viral pericarditis . 13 Aetiology and classification of pericardial disease. 2 Bacterial pericarditis . 14 Pericardial syndromes . ..................... 2 Tuberculous pericarditis . 14 Congenital defects of the pericardium . 2 Pericarditis in renal failure . 16 Acute pericarditis . 2 Autoreactive pericarditis and pericardial Chronic pericarditis . 6 involvement in systemic autoimmune Recurrent pericarditis . 6 diseases . 16 Pericardial effusion and cardiac tamponade .
    [Show full text]
  • Essentials of Bedside Cardiology CONTEMPORARY CARDIOLOGY
    Essentials of Bedside Cardiology CONTEMPORARY CARDIOLOGY CHRISTOPHER P. CANNON, MD SERIES EDITOR Aging, Heart Disease and Its Management: Facts and Controversies, edited by Niloo M. Edwards, MD, Mathew S. Maurer, MD, and Rachel B. Wellner, MD, 2003 Peripheral Arterial Disease: Diagnosis and Treatment, edited by Jay D. Coffman, MD, and Robert T. Eberhardt, MD, 2003 Essentials ofBedside Cardiology: With a Complete Course in Heart Sounds and Munnurs on CD, Second Edition, by Jules Constant, MD, 2003 Primary Angioplasty in Acute Myocardial Infarction, edited by James E. Tcheng, MD,2002 Cardiogenic Shock: Diagnosis and Treatment, edited by David Hasdai, MD, Peter B. Berger, MD, Alexander Battler, MD, and David R. Holmes, Jr., MD, 2002 Management of Cardiac Arrhythmias, edited by Leonard I. Ganz, MD, 2002 Diabetes and Cardiovascular Disease, edited by Michael T. Johnstone and Aristidis Veves, MD, DSC, 2001 Blood Pressure Monitoring in Cardiovascular Medicine and Therapeutics, edited by William B. White, MD, 2001 Vascular Disease and Injury: Preclinical Research, edited by Daniell. Simon, MD, and Campbell Rogers, MD 2001 Preventive Cardiology: Strategies for the Prevention and Treatment of Coronary Artery Disease, edited by JoAnne Micale Foody, MD, 2001 Nitric Oxide and the Cardiovascular System, edited by Joseph Loscalzo, MD, phD and Joseph A. Vita, MD, 2000 Annotated Atlas of Electrocardiography: A Guide to Confident Interpretation, by Thomas M. Blake, MD, 1999 Platelet Glycoprotein lIb/IlIa Inhibitors in Cardiovascular Disease, edited by A. Michael Lincoff, MD, and Eric J. Topol, MD, 1999 Minimally Invasive Cardiac Surgery, edited by Mehmet C. Oz, MD and Daniel J. Goldstein, MD, 1999 Management ofAcute Coronary Syndromes, edited by Christopher P.
    [Show full text]
  • Systolic Murmurs
    Murmurs and the Cardiac Physical Exam Carolyn A. Altman Texas Children’s Hospital Advanced Practice Provider Conference Houston, TX April 6 , 2018 The Cardiac Physical Exam Before applying a stethoscope….. Some pearls on • General appearance • Physical exam beyond the heart 2 Jugular Venous Distention Pallor Cyanosis 3 Work of Breathing Normal infant breathing Quiet Tachypnea Increased Rate, Work of Breathing 4 Beyond the Chest Clubbing Observed in children older than 6 mos with chronic cyanosis Loss of the normal angle of the nail plate with the axis of the finger Abnormal sponginess of the base of the nail bed Increasing convexity of the nail Etiology: ? sludging 5 Chest ❖ Chest wall development and symmetry ❖ Long standing cardiomegaly can lead to hemihypertrophy and flared rib edge: Harrison’s groove or sulcus 6 Ready to Examine the Heart Palpation Auscultation General overview Defects Innocent versus pathologic 7 Cardiac Palpation ❖ Consistent approach: palm of your hand, hypothenar eminence, or finger tips ❖ Precordium, suprasternal notch ❖ PMI? ❖ RV impulse? ❖ Thrills? ❖ Heart Sounds? 8 Cardiac Auscultation Where to listen: ★ 4 main positions ★ Inching ★ Ancillary sites: don’t forget the head in infants 9 Cardiac Auscultation Focus separately on v Heart sounds: • S2 normal splitting and intensity? • Abnormal sounds? Clicks, gallops v Murmurs v Rubs 10 Cardiac Auscultation Etiology of heart sounds: Aortic and pulmonic valves actually close silently Heart sounds reflect vibrations of the cardiac structures after valve closure Sudden
    [Show full text]
  • Hemodynamic Assessment of Pneumopericardium by Echocardiography
    Extended Abstract Haemodynamics, deformation & ischaemic heart disease Hemodynamic assessment of pneumopericardium by echocardiography Matias Trbušić* KEYWORDS: pneumopericardium, cardiac tamponade, pericardiocentesis. CITATION: Cardiol Croat. 2017;12(4):124. | https://doi.org/10.15836/ccar2017.124 University Hospital Centre * “Sestre milosrdnice”, Zagreb, ADDRESS FOR CORRESPONDENCE: Matias Trbušić, Klinički bolnički centar Sestre milosrdnice, Vinogradska 29, Croatia HR-10000 Zagreb, Croatia. / Phone: +385-91-506-2986 / E-mail: [email protected] ORCID: Matias Trbušić, http://orcid.org/0000-0001-9428-454X Background: Pneumopericardium is a rare condition de- fined as a collection of air in the pericardial cavity. It is usually result of chest injuries, iatrogenic causes (bone marrow puncture, thoracic surgery, pericardiocentesis, endoscopic procedures), and infective agents causing pu- rulent gas - producing pericarditis.1,2 Case report: We represent a case of 82-year old female pa- tient with spontaneous pneumopericardium caused by malignant ulcer that created fistula between the pericar- dium and colon. She was admitted in very severe condi- tion with chest pain, severe respiratory distress, hypoten- sion, distended neck veins and tachyarrhythmia. High blood leukocyte, high C reactive protein levels and com- bined respiratory and metabolic acidosis were present. Electrocardiogram showed atrial fibrillation and diffuse micro voltage. Chest X ray and CT showed normal sized heart surrounded by air (halo sign) below the aortic arch, and large left pleural effusion. CT also revealed neoplastic process of the transverse colon infiltrating stomach and diaphragm. Due to intrapericardial spontaneous contrast echoes the image quality of 2-D echocardiography was poor making difficult to verify signs typical for tampon- ade such as early diastolic right ventricular collapse and early diastolic right atrial collapse (Figure 1).
    [Show full text]
  • Case Report on Dressler's Syndrome
    ical C lin as Jasmina et al., J Clin Case Rep 2018, 8:4 C e f R o l e DOI: 10.4172/2165-7920.10001106 a p n o r r t u s o J Journal of Clinical Case Reports ISSN: 2165-7920 Case Report Open Access Case Report on Dressler’s Syndrome Jasmina Ek1*, Lisa Mary Koshy2 and Anjali Kuriakose3 Department of Pharmacy, National College of Pharmacy Kozhikode, Kerala, India Abstract Introduction: Dressler’s syndrome (delayed pericarditis) is considered as a secondary form of pericarditis resulting in the inflammation of the sac surrounding heart (pericardium). Case Presentation: A 56-year-old male was admitted to the cardiology department due to left sided chest pain associated with breathlessness, palpitation and sweating. patient had a past history of CAD-AWMI, moderate left ventricular(LV) dysfunction (diagnosed 2 months back). Percutaneous transluminal coronary angioplasty (PTCA) with stent to CAD done 2 months back. ECHO shows mild to moderate pericardial effusion, mild pulmonary arterial hypertension(PAH), moderate mitral regurgitation (MR), moderate LV dysfunction. Conclusion: This reveals that the patient is diagnosed with Dressler’s syndrome, a rare disease in the age of reperfusion therapy. Keywords: Myocardial infarction; Pericarditis; Chest pain; Dressler’s hypertension (PAH), moderate mitral regurgitation (MR), moderate LV syndrome dysfunction. Introduction The incidence of this condition is declining with improved reperfusion therapy after myocardial infarction (5). The CKMB was Dressler’s syndrome also known as post myocardial infarction almost normal (21.6 IU/L) and the troponin I shows negative (0.01 syndrome, is a form of secondary pericarditis with or without ng/mL), The echocardiogram showed evidence of pericardial effusion, a pericardial effusion, that occurs because of injury to heart or which is mandatory for the diagnosis of pericarditis.
    [Show full text]
  • Pneumopericardium and Tension Pneumopericardium After Closed-Chest Injury
    Thorax: first published as 10.1136/thx.32.1.91 on 1 February 1977. Downloaded from Thorax, 1977, 32, 91-97 Pneumopericardium and tension pneumopericardium after closed-chest injury S. WESTABY From Papworth Hospital, Cambridge Westaby, S. (1977). Thorax, 32, 91-97. Pneumopericardium and tension pneumopericardium after closed-chest injury. Three recent cases of pneumopericardium after closed-chest injury are described. The mechanism of pericardial inflation suspected in each was pleuropericardial laceration in the presence of an intrathoracic air leak. Deflation of the pericardium was achieved by underwater seal drainage of the right pleural cavity in the first patient, during thoracotomy for repair of tracheobronchial rupture-in the second, and by subxiphoid pericardiotomy in the last. Haemodynamic changes after escape of air from the pericardium of the second patient confirmed the existence of tension pneumopericardium and air tamponade. Pneumopericardium after a non-penetrating chest click. The right chest was resonant with decreased injury is rare. There are few previous reports of breath sounds. Precordial auscultation revealed a this lesion, and in the presence of additional in- loud splashing sound or 'bruit de moulin'. Chest jury its clinical importance remains poorly defined. radiographs demonstrated a large pneumopericar- This paper examines three recent cases in which dium and a 50% pneumothorax on the right, with operative deflation of the pericardium was per- no mediastinal shift. Needle aspiration of the http://thorax.bmj.com/ formed. In one case release of air resulted in pericardium was performed through the fourth marked haemodynamic changes leading to a left interspace and 40 ml of air with frothy blood diagnosis of tension pneumopericardium.
    [Show full text]
  • Pub 100-04 Medicare Claims Processing Centers for Medicare & Medicaid Services (CMS) Transmittal 3054 Date: August 29, 2014 Change Request 8803
    Department of Health & CMS Manual System Human Services (DHHS) Pub 100-04 Medicare Claims Processing Centers for Medicare & Medicaid Services (CMS) Transmittal 3054 Date: August 29, 2014 Change Request 8803 SUBJECT: Ventricular Assist Devices for Bridge-to-Transplant and Destination Therapy I. SUMMARY OF CHANGES: This Change Request (CR) is effective for claims with dates of service on and after October 30, 2013; contractors shall pay claims for Ventricular Assist Devices as destination therapy using the criteria in Pub. 100-03, part 1, section 20.9.1, and Pub. 100-04, Chapter 32, sec. 320. EFFECTIVE DATE: October 30, 2013 *Unless otherwise specified, the effective date is the date of service. IMPLEMENTATION DATE: September 30, 2014 Disclaimer for manual changes only: The revision date and transmittal number apply only to red italicized material. Any other material was previously published and remains unchanged. However, if this revision contains a table of contents, you will receive the new/revised information only, and not the entire table of contents. II. CHANGES IN MANUAL INSTRUCTIONS: (N/A if manual is not updated) R=REVISED, N=NEW, D=DELETED-Only One Per Row. R/N/D CHAPTER / SECTION / SUBSECTION / TITLE D 3/90.2.1/Artifiical Hearts and Related Devices R 32/Table of Contents N 32/320/Artificial Hearts and Related Devices N 32/320.1/Coding Requirements for Furnished Before May 1, 2008 N 32/320.2/Coding Requirements for Furnished After May 1, 2008 N 32/320.3/ Ventricular Assist Devices N 32/320.3.1/Postcardiotomy N 32/320.3.2/Bridge-To -Transplantation (BTT) N 32/320.3.3/Destination Therapy (DT) N 32/320.3.4/ Other N 32/320.4/ Replacement Accessories and Supplies for External Ventricular Assist Devices or Any Ventricular Assist Device (VAD) III.
    [Show full text]
  • View Pdf Copy of Original Document
    Phenotype definition for the Vanderbilt Genome-Electronic Records project Identifying genetics determinants of normal QRS duration (QRSd) Patient population: • Patients with DNA whose first electrocardiogram (ECG) is designated as “normal” and lacking an exclusion criteria. • For this study, case and control are drawn from the same population and analyzed via continuous trait analysis. The only difference will be the QRSd. Hypothetical timeline for a single patient: Notes: • The study ECG is the first normal ECG. • The “Mildly abnormal” ECG cannot be abnormal by presence of heart disease. It can have abnormal rate, be recorded in the presence of Na-channel blocking meds, etc. For instance, a HR >100 is OK but not a bundle branch block. • Y duration = from first entry in the electronic medical record (EMR) until one month following normal ECG • Z duration = most recent clinic visit or problem list (if present) to one week following the normal ECG. Labs values, though, must be +/- 48h from the ECG time Criteria to be included in the analysis: Criteria Source/Method “Normal” ECG must be: • QRSd between 65-120ms ECG calculations • ECG designed as “NORMAL” ECG classification • Heart Rate between 50-100 ECG calculations • ECG Impression must not contain Natural Language Processing (NLP) on evidence of heart disease concepts (see ECG impression. Will exclude all but list below) negated terms (e.g., exclude those with possible, probable, or asserted bundle branch blocks). Should also exclude normalization negations like “LBBB no longer present.”
    [Show full text]
  • Constriction Versus Restriction Anurag Bajaj. MD Regional Health
    10/21/2019 Constriction versus Restriction Anurag Bajaj. MD Regional Health Recognizing constrictive pericarditis and restrictive cardiomyopathy as a reversible cause of heart failure. Understand the pathophysiology of constrictive pericarditis and restrictive cardiomyopathy. Echocardiographic findings differentiating between constrictive pericarditis and restrictive cardiomyopathy. Invasive hemodynamics findings differentiating between constrictive pericarditis and restrictive cardiomyopathy. 1 10/21/2019 A 45-year-old man is evaluated for a 6-month history of progressive dyspnea on exertion and lower- extremity edema. He can now walk only one block before needing to rest. He reports orthostatic dizziness in the last 2 weeks. He was diagnosed 15 years ago with non-Hodgkin lymphoma, which was treated with chest irradiation and chemotherapy and is now in remission. He also has type 2 diabetes mellitus. He takes furosemide (80 mg, 3 times daily), glyburide, and low-dose aspirin. Physical examination Afebrile. Blood pressure of 125/60 mm Hg supine and 100/50 mm Hg standing; pulse is 90/min supine and 110/min standing. Respiration rate is 23/min. BMI is 28. Presence of jugular venous distention and jugular venous engorgement with inspiration. CVP of 15 cm H2O. Cardiac examination discloses diminished heart sounds and a prominent early diastolic sound but no gallops or murmurs. Pulmonary auscultation discloses normal breath sounds and no crackles. Abdominal examination shows shifting dullness Lower extremities show 3+ pitting edema to the level of the knees. Remainder of the physical examination is normal. BUN 40 mg/dL, Cr 2.0 mg/dL, ALT 130 U/L, AST 112 U/L, Albumin 3.0 g/dL, UA negative for protein, 2 10/21/2019 70 year old female presented with dyspnea caused by minor stress.
    [Show full text]
  • Pregnancy and Cardiovascular Disease
    Pregnancy and Cardiovascular Disease Cindy M. Martin, M.D. Co-Director, Adult Congenital and Cardiovascular Genetics Center No Disclosures Objectives • Discuss the hemodynamic changes during pregnancy • Define the low, medium and high risk cardiac lesions as related to pregnancy • Review use of cardiovascular drugs in pregnancy Pregnancy and the Heart • 2-4% of pregnancies in women without preexisting cardiac abnormalities are complicated by maternal CV disease • In 2000, there were an estimated 1 million adult patients in the US with congenital heart disease (CHD), with the number increasing by 5% yearly • In 2005, the number of adult patients with CHD surpassed the number of children with CHD in the United States • CV and CHD disease does not always preclude pregnancy but may pose increase risk to mother and fetus Hemodynamic Changes during Pregnancy • Blood Volume – increases 40-50% • Heart rate – increases 10-15 bpm • SVR and PVR – decreases • Blood Pressure – decreases 10mmHg • Cardiac Output – increases 30-50% – Peaks at end of second trimester and plateaus until delivery • These changes are usually well tolerated Physiologic Changes in Pregnancy Hemodynamic Changes in Labor and Delivery • CO increases an additional 50% with each contraction – Uterine contraction displaces 300-500ml blood into the general circulation – Possible for the cardiac output to be 70-80% above baseline during labor and delivery • Mean arterial pressure also usually rises • Volume changes – Increased blood volume with uterine contraction – Increase venous
    [Show full text]
  • 2015 ESC Guidelines for the Diagnosis and Management Of
    European Heart Journal Advance Access published August 29, 2015 European Heart Journal ESC GUIDELINES doi:10.1093/eurheartj/ehv318 2015 ESC Guidelines for the diagnosis and management of pericardial diseases The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC) Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS) Downloaded from Authors/Task Force Members: Yehuda Adler* (Chairperson) (Israel), Philippe Charron* (Chairperson) (France), Massimo Imazio† (Italy), Luigi Badano (Italy), Gonzalo Baro´ n-Esquivias (Spain), Jan Bogaert (Belgium), Antonio Brucato http://eurheartj.oxfordjournals.org/ (Italy), Pascal Gueret (France), Karin Klingel (Germany), Christos Lionis (Greece), Bernhard Maisch (Germany), Bongani Mayosi (South Africa), Alain Pavie (France), Arsen D. Ristic´ (Serbia), Manel Sabate´ Tenas (Spain), Petar Seferovic (Serbia), Karl Swedberg (Sweden), and Witold Tomkowski (Poland) Document Reviewers: Stephan Achenbach (CPG Review Coordinator) (Germany), Stefan Agewall (CPG Review Coordinator) (Norway), Nawwar Al-Attar (UK), Juan Angel Ferrer (Spain), Michael Arad (Israel), Riccardo Asteggiano (Italy), He´ctor Bueno (Spain), Alida L. P. Caforio (Italy), Scipione Carerj (Italy), Claudio Ceconi (Italy), Arturo Evangelista (Spain), Frank Flachskampf (Sweden), George Giannakoulas (Greece), Stephan Gielen by guest on October 21, 2015 (Germany), Gilbert Habib (France), Philippe Kolh (Belgium), Ekaterini Lambrinou (Cyprus), Patrizio Lancellotti (Belgium), George Lazaros (Greece), Ales Linhart (Czech Republic), Philippe Meurin (France), Koen Nieman (The Netherlands), Massimo F. Piepoli (Italy), Susanna Price (UK), Jolien Roos-Hesselink (The Netherlands), * Corresponding authors: Yehuda Adler, Management, Sheba Medical Center, Tel Hashomer Hospital, City of Ramat-Gan, 5265601, Israel. Affiliated with Sackler Medical School, Tel Aviv University, Tel Aviv, Israel, Tel: +972 03 530 44 67, Fax: +972 03 530 5118, Email: [email protected].
    [Show full text]
  • Cardiac Valvular Disease
    CARDIOLOGY II: Cardiac Valvular Disease Ischemic Heart Disease Congenital Heart Disease (Adult presentations) Vascular Disease Rutgers PANCE/PANRE Review Course Cardiac Valvular Disease Aortic – Stenosis and Regurgitation Pulmonic Mitral Tricuspid Rutgers PANCE/PANRE Review Course Cardiac Valvular Disease Historically in US – Rheumatic in origin Still true in developing countries Now, atherosclerosis involved ? Genetic markers with AS ? Many patients are s/p surgical intervention ECHO remains best diagnostic tool Rutgers PANCE/PANRE Review Course Valvular Dz Practice Case A 22 y/o waitress presents c/o generalized, sub-sternal chest pain that is worsened with exertion. She appears anxious; she denies ETOH, tobacco, and illicit drug use. You auscultate her heart and diagnose MVP. What did you hear to make this diagnosis? Rutgers PANCE/PANRE Review Course Choices: A. A diastolic rumble B. A holo-systolic murmur C. A midsystolic click D. An opening snap Rutgers PANCE/PANRE Review Course Answer: A. A diastolic rumble B. A holo-systolic murmur C. A midsystolic click D. An opening snap Rutgers PANCE/PANRE Review Course Valvular Disease Basics Four Valves: Two main conditions: Aortic Stenosis Mitral Regurgitation or Tricuspid insufficiency Pulmonic Rutgers PANCE/PANRE Review Course Valvular Disease - localization nd Aortic area: 2 R interspace nd Pulmonic area: 2 L interspace Tricuspid area: LLSB Mitral area: Apex (Think APT. Ment — going from right to left along patient’s chest) Rutgers PANCE/PANRE Review Course The Aortic Valve www.healcentral.org UMDNJ PANCE/PANRERutgers Review CoursePANCE/PANRE (becoming Rutgers Review July 1, 2013) Course Aortic Stenosis (AS) 2 ‘routes of entry’/causes possible: Uni/bicuspid aortic valve (congenital) often presents at 50-65 y/o Degenerative or calcific aortic valve o Results from calcium deposits 2 to atherosclerosis (Genetic markers associated: “Notch 1”) So .
    [Show full text]