3-Valvular Heart Diseases (VHD).Pdf
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1. Intermittent Chest Pain: Angina: • Stable: (Caused By
CVS: 1. Intermittent chest pain: Angina: • Stable: (caused by chronic narrowing in one or more coronary arteries), episodes of pain are precipitated by exertion and may occur more readily when walking in cold or windy weather, after a large meal or while carrying a heavy load; the pain is promptly relieved by rest and/or sublingual glyceryl nitrate (GTN) spray, and typically lasts for less than 10 minutes. • unstable angina (caused by a sudden severe narrowing in a coronary artery), there is usually an abrupt onset or worsening of chest pain episodes that may occur on minimal exertion or at rest. • Retrosternal/ Progressive onset/ increase in intensity over 1–2 minutes/ Constricting, heavy/ Sometimes arm(s), neck, epigastrium/ Associated with breathlessness/ Intermittent, with episodes lasting 2–10 minutes/ Triggered by emotion, exertion, especially if cold, windy/ Relieved by rest, nitrates Mild to moderate. • Aggravated by thyroxine or drug-induced anemia, e.g. aspirin or NSAIDs Esophageal: • Retrosternal or epigastric/ Over 1–2 minutes; can be sudden (spasm)/ C: Gripping, tight or burning/ R: Often to back, sometimes to arms/ A: Heartburn, acid reflux/ T: Intermittent, often at night-time; variable duration/ Lying flat/some foods may trigger/ Not relieved by rest; nitrates sometimes relieve/ Usually mild but esophageal spasm can mimic myocardial infarction. 2. Acute chest pain: MI: • SOCRATES: Retrosternal/ Rapid over a few minutes/ Constricting, heavy/ Often to arm(s), neck, jaw, sometimes epigastrium/ Sweating, nausea, vomiting, breathlessness, feeling of impending death (angor animi)/ Acute presentation; prolonged duration/ ’Stress’ and exercise rare triggers, usually spontaneous/ Not relieved by rest or nitrates/ Usually severe. -
Valvular Heart Disease Acute Rheumatic Fever
Valvular heart disease Acute rheumatic fever Rheumatic fever • It typically occurs several weeks after streptococcal pharyngitis. • The most common pathogen is group A beta-hemolytic streptococci (GABHS) • Streptococcus cross-react with proteins in cardiac valves. • Time from acute streptococcal infection to onset of symptomatic rheumatic fever (RF) is usually 3–4 weeks. • RF is thought to complicate up to 3% of untreated streptococcal sore throats. • Previous episodes of RF predispose to recurrences. Diagnostic criteria for rheumatic fever (Jones criteria) • Evidence of group A streptococcal pharyngitis • Either a positive throat culture or rapid streptococcal antigen test, or an elevated or rising streptococcal antibody titer (samples taken 2 weeks apart). • Plus two major or one major and two minor Jones criteria: Major criteria Minor criteria • Polyarthritis • Fever • Carditis • Arthralgia • Chorea • Prolonged PR interval • Erythema marginatum • Elevated ESR and CRP • Subcutaneous nodules Joints • Migratory large-joint polyarthritis starting in the lower limbs in 75% of cases. Duration is <4 weeks at each site. There is severe pain and tenderness in contrast to a mild degree of joint swelling. Heart • Pancarditis occurs in 50% of cases with features of acute heart failure, mitral and aortic regurgitation, and pericarditis. • Endocarditis • affects the mitral valve (65%–70%), aortic valve (25%), and tricuspid valve (10%, never in isolation), causing acute regurgitation and heart failure but chronic stenosis. • Pericarditis • Pain • Friction rub • rarely causes hemodynamic instability/tamponade or constriction. Heart Myocarditis • Acute heart failure • Arrhythmias • Most common reason of death Skin • Erythema marginatum is an evanescent rash with serpiginous outlines and central clearings on the trunk and proximal limbs. -
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 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 Recognition and Management of Valvular Heart Disease
VALVULAR HEART DISEASE THE RECOGNITION AND MANAGEMENT OF VALVULAR HEART DISEASE Discussion of heart murmurs tends to be associated with specialist ward rounds in teaching hospitals, but a good understanding of this clinical sign provides valuable information. AUSCULTATING A HEART MURMUR When does it occur? •Time the murmur in systole or diastole to the first heart sound and by palpating the upstroke of the carotid artery as systole. • Is the murmur early, mild, late, holosystolic, or diastolic? How loud is it? •Grade I — very soft, only heard with special effort • Grade II — soft, faint, but heard immediately • Grade III — moderately loud • Grade IV — so loud that a thrill can be felt •Grade V — very loud, heard with only part of the stethoscope on the chest wall J A KER • Grade VI — heard with the stethoscope removed from the chest wall. MB ChB, MMed (Int), MD Professor Where is it maximal? Department of Internal Medicine • Apex, left parasternal area, aortic area, pulmonary area. School of Medicine Where does it radiate to? University of Pretoria • Neck, axilla, back. Categories of heart murmurs There are three broad categories of heart murmurs: • systolic (murmur begins with S1 or after S1, ends at S2) • diastolic (murmur begins after S2, ends before S1) • continuous (murmur continues without interruption from systole through S2 into diastole. Typical in patent ductus arteriosus). Systolic heart murmurs Systolic murmurs are illustrated in Fig. 1 and are classified as: • early systolic • midsystolic •late systolic • holosystolic (pansystolic) Early systolic murmurs occur in acute severe mitral regurgitation, tricuspid regurgitation (with normal right ventricular (RV) pressures) and ventricular septal defect (VSD). -
12 ACE (Angiotensin-Converting Enzyme)
Index Ablation, radiofrequency, 58–59 Antihypertensive and Lipid Ablative therapy, 65–66 Lowering Treatment to Accupril (quinapril), 12 Prevent Heart Attack Trial ACE (angiotensin-converting (ALLHAT), 18 enzyme) inhibitors, 7 Antihypertensive drug classes, Acebutolol (Sectral), 13, 61 7–18 Aceon (perindopril), 13 Antihypertensive drug selection, Adalat Procardia (nifedipine), 14 19–20 Adenocard (adenosine), 64 Antihypertensive drugs, 12–16 Adenosine (Adenocard), 64 Antiplatelet therapy, 40 Adolescents Aortic insufficiency, 98–99 sudden cardiac death in, 218–219 Aortic stenosis, 105–107 syncope in, 213 Aspirin Alcohol, 158 angina pectoris and, 36 Aldactone (spironolactone), 16 low-dose, 188 Aldomet (methyldopa), 15 Atenolol (Tenormin), 13, 61 ab-blockers, 15 Atherosclerosis, 186–187 a1-blockers, 14, 17 premature, 148–149 Altace (ramipril), 13 Athletes Amiloride (Midamor), 15 murmurs in, 111–112 Amiodarone (Cordarone), 63 sudden cardiac death in, 219–220 Amlodipine (Norvasc), 14 Atorvastatin (Lipitor), 163 Aneurysm, 196–197 Atrial fibrillation, 191–192, 76–80 Angina pectoris, 27–28, 32–41 Atrial flutter, 80–81 aspirin and, 36 Atrial premature beats, 70 unstable, 36–41 Atrial tachycardia, 73 Angiotensin-converting enzyme Atrioventricular (AV) nodal (ACE) inhibitors, 7 reentrant tachycardias, 74–75 Angiotensin receptor antagonists, Atrioventricular node, 53 9 Atrioventricular reciprocating Ankle-brachial index, 282 tachycardias, 75–76 Antiadrenergic agents, 11–18 Austin Flint murmur, 104 Antiarrhythmic drugs, 59–65 AV, see Atrioventricular -
Cardiovascular Semiotics: the Personalities Behind the Eponyms
International Journal of Cardiovascular Sciences. 2016;29(5):396-406 396 REVIEW ARTICLE Cardiovascular Semiotics: The Personalities Behind the Eponyms Renata Gudergues Pereira de Almeida1, Juliana dos Santos Macaciel1, Érico Araújo Reis Santos1, Thiago Calvet Cavalcanti Garcia1, Anastacia Midori Hashimoto1, Cláudio Tinoco Mesquita1,2 Departamento de Medicina Clínica – Faculdade de Medicina – Universidade Federal Fluminense1, Programa de Pós-Graduação em Ciências Cardiovasculares da UFF2, Niterói, RJ – Brazil Abstract observed in life today is also present in medicine and its teaching. Currently, many teachers and students Since its inception, medicine has been based tend to neglect cardiac auscultation in favor of on observation of signs and specific findings in ill imaging examinations to evaluate the heart, such as patients. Semiotics is, therefore, an ancient study. echocardiography and magnetic resonance imaging. Cardiac semiology, although more recent, is more However, it is worth noting that, in many cases, the complex in its learning due to difficulties in the reality of medicine distances patients from access interpretation of auscultatory findings. Austin Flint, to cardiovascular imaging examinations, even in Rivero Carvallo, Antonio Valsalva, and Adolf Kussmaul large centers. are some of the many physicians who have dedicated The lack of competence for cardiac auscultation themselves to the academic study of cardiac semiology can be seen in several countries around the world. and became eternalized in the medical field through -
PANCE/PANRE Review Course 1/20/2016 1
PANCE/PANRE Review Course 1/20/2016 Cardiology II Presented by Carol J. Sadley, M.Ed., PA-C Rutgers University Physician Assistant Certification and Recertification Examination Review Course June 2, 2015 Rutgers, The State University of New Jersey PANCE/PANRE Review Course Cardiology II • Cardiac Valvular Disease • Ischemic Heart Disease •Cong(genital Heart Disease (Adult presentations) • Vascular Disease PANCE/PANRE Review Course Cardiac Valvular Disease • Aortic – Stenosis and Regurgitation • Pulmonic • Mitral • Tricuspid 1 PANCE/PANRE Review Course 1/20/2016 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 PANCE/PANRE Review Course Valvular Disease 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? A. A diastolic rumble A. A diastolic rumble B. A holo-systolic murmur B. A holo-systolic murmur C. A midsystolic click C. A midsystolic click D. An opening snap D. An opening snap PANCE/PANRE Review Course Valvular Disease Basics Four Valves: Two main conditions: •Aortic • Stenosis • Mitral • Regurgitation or • Tricuspid insufficiency • Pulmonic 2 PANCE/PANRE Review Course 1/20/2016 PANCE/PANRE Review Course -
A Case of Dyspnoea and Visible Neck Pulsations
Online image challenge A case of dyspnoea and visible orthopnoea and palpitations. The symptom aggravation was Heart: first published as 10.1136/heartjnl-2015-308831 on 13 January 2016. Downloaded from abrupt with simultaneous occurrence of both dyspnoea and neck pulsations palpitations. After medical stabilisation, the neck pulsations were as shown in online supplementary video 1. QUESTION What is the most likely cardiac condition? CLINICAL INTRODUCTION A. Aortic regurgitation A 48-year-old male patient with a history of New York Heart B. Congestive cardiac failure Association (NYHA) Class II dyspnoea for the last 2 years C. Tricuspid regurgitation presented with acute onset breathlessness associated with D. Ventricular tachycardia http://heart.bmj.com/ on September 30, 2021 by guest. Protected copyright. Benny PJ, et al. Heart March 2016 Vol 102 No 6 e1 Online image challenge ANSWER: A visible at the root of the neck and no periodicity of pairs as Heart: first published as 10.1136/heartjnl-2015-308831 on 13 January 2016. Downloaded from The major clue here is to find out whether it is an arterial noted in this video. pulsation or a venous pulsation. Typically, an elevated jugular venous pulse ( JVP) will be equally or more prominent at the Panakkal Jose Benny, Gopalan Nair Rajesh, Chakkanalil Govindan Sajeev root of the neck and will show an upper level. The descents Department of Cardiology, Government Medical College, Kozhikode, Kerala, India will be more prominent than the outward pulsations.1 On Correspondence to Dr Panakkal Jose Benny, Senior Resident, Department of the contrary, arterial neck pulsations will be most prominent Cardiology, Government Medical College, Kozhikode 673008, Kerala, India; at the mid-neck level with little or no appreciable pulsation [email protected] at the root of the neck. -
Quick Guide to Cardiopulmonary Care
Edwards Clinical Education Quick Guide to Cardiopulmonary Care 4th Edition This reference guide is presented as an aide to guide medical personnel by Edwards Lifesciences. The information in this reference guide has been compiled from available literature. Although every effort has been made to report faithfully the information, the editors and publisher cannot be held responsible for the correctness. This guide is not intended to be, and should not be construed as, medical advice. For any use, the product information guides, inserts and operation manuals of the various drugs and devices should be consulted. Edwards Lifesciences and the editors disclaim any liability arising directly or indirectly from the use of drugs, devices, techniques or procedures described in this reference guide. Note: Algorithms and protocols included in this book are for educational reference only. Edwards does not endorse or support any one specific algorithm or protocol. It is up to each individual clinician and institution to select the treatment that is most appropriate. ISBN 978-0-615-96605-2 Quick Guide to Cardiopulmonary Care 4th Edition Editors William T. McGee, MD, MHA, FCCP, FCCM Critical Care Medicine Associate Professor of Medicine and Surgery University of Massachusetts Medical School Caulette Young, BSN, RN, CCRN, CHSE Clinical Nurse Consultant John A. Frazier, BS, RN, RRT Sr. Manager Edwards Lifesciences Previous edition editor Peter R. Lichtenthal, M.D. Previous editions contributors and reviewers Diane K. Brown, RN, MSN, CCRN Barbara “Bobbi” Leeper, MN, RN, CCRN Quick Guide to Cardiopulmonary Care Pertinent clinical information dedicated to the critical care clinician The intent of the Quick Guide is to provide a ready reference for hemodynamic monitoring and oxygenation assessment of the critically ill. -
Pulse 1 Pulse
Pulse 1 Pulse In medicine, a person's pulse is the arterial palpation of a heartbeat.[1] It can be felt in any place that allows for an artery to be compressed against a bone, such as at the neck (carotid artery), at the wrist (radial artery), behind the knee (popliteal artery), on the inside of the elbow (brachial artery), and near the ankle joint (posterior tibial artery). The pulse rate can also be measured by measuring the heart beat directly (auscultation), usually using a stethoscope. Physiology The pulse is a decidedly low tech/high yield and antiquated term still useful at the bedside in an age of computational analysis of cardiac performance. Claudius Galen (129AD?) was perhaps the first physiologist to describe the pulse. The pulse is an expedient tactile method of determination of systolic blood pressure to a trained observer. Diastolic blood pressure is non-palpable and unobservable, occurring between heartbeats. Pressure waves generated by cardiac systole move the artery walls, which are pliable and compliant. These properties form enough to create a palpable pressure wave. The heart rate can be (much) higher than the pulse rate depending upon the cause or etiology. In this case, the heart rate is determined by auscultation of the heart apex, in which case it is not the pulse. The pulse deficit (difference between heart beats and pulsations at the periphery) is determined by simultaneous palpation at the radial artery and auscultation at the heart apex. Pulse velocity, pulse deficits and much more physiologic data is readily and simplistically visualized by the use of one or more arterial catheters connected to a transducer and oscilloscope. -
Represented, but the Latter, Instead Or Being Rounded Muscles ; Both Rise and Fall Are Rapid and the Line of the and Sustained, Forms a Sharp Angle
1529 begun aouve at the tlllH1 1-10, and transvetsely Excended from ON THE PULSUS BISFERIENS OF AORTIC the right border of the sternum to a point nearly one inch to REGURGITATION.1 the left beyond the posirjon of the maximum Impulse. A long, soft diastolic murmur in the aortic area entirely replaced the MICHELL M.D. BY J. CLARKE, M A, CAMB., aortic second sound, aLd was conducted upwards but more M.R.C.P. LOND., distinctly downwards along the left border of the sternum, PHYSICIAN TO THE GENERAL HOSPITAL, AND LECTURER ON PRACTICAL and was audible at the apex. the first sound at the PHYSIOLOGY, UNIVERSITY BRISTOL. COLLEGE, apex was indistinct, and sometimes during his stay in hospital a systol’c murmur appealed there. No systolic SHORTLY after reading the very instructive and interest- murmur was heard at the base. The pulmonary second ing papers of Dr. Graham Steell on this subject,2 and sound was feeble. There was a little dulness at the base of the left and the liver and were both to which I here express my indebtedness, a well-marked lung, fpleen There was no and the urine did not contain of the somewhat rare of this described enlarged. dropsy .example type pulse albumen. A cardiographic tracing at this time, taken him came under own observation. This of by my variety over the seat of the maximum ventricular impulse, showed pulse is generally described as a form produced by aortic delay in the pulse wave (only an indication and not a good stenosis, but occurring much more rarely than the more tracing of the brachial pulse was obtained) ; in the ventri- cisual modification of the pulse found in this lesion-namely, cular curve the rise due to the auricle was well marked, and a the anacrotic pulse.