DOCSLIB.ORG

Pericardial Diseases

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pericardial Diseases PERICARDIAL DISEASES Kruti Pandya MD LEARNING OBJECTIVES: 1. Understand the function and description of the pericardium. 2. Identify the diagnostic criteria and etiologies of acute pericarditis, pericardial effusion and constrictive pericarditis. 3. Understand the hemodynamic consequences of pericardial effusion and constrictive pericarditis. 4. Integrate the information obtained from a history, physical examination, electrocardiography, and laboratory studies to determine the diagnosis of the various pericardial syndromes. 5. Understand the treatment strategies to decrease morbidity and improve survival in patients with pericardial disease based on the basis of evidence and clinical experience PERICARDIUM: ANATOMY • Pericardial Layers: • Visceral layer • Parietal layer • Fibrous pericardium • Between the two layers lies the pericardial space, which contains approximately 10-50ml of fluid, which is an ultrafiltrate of plasma. FUNCTION OF THE PERICARDIUM • 1. Stabilization of the heart within the thoracic cavity by virtue of its ligamentous attachments -- limiting the heart’s motion. • 2. Protection of the heart from mechanical trauma and infection from adjoining structures. • 3. The pericardial fluid functions as a lubricant and decreases friction of cardiac surface during systole and diastole. • 4. Prevention of excessive dilation of heart especially during sudden rise in intra-cardiac volume (e.g. acute aortic or mitral regurgitation). PERICARDIAL DISEASES • Acute pericarditis • Pericardial effusion, Cardiac Tamponade. • Chronic constrictive pericarditis. ACUTE PERICARDITIS: • Common • Inflammation of layers of pericardium • 0.1% of hosp. pts ; 5% of ER pts with diagnosed with noncardiac chest pain. ETIOLOGY OF ACUTE PERICARDITIS • INFECTIVE • NEOPLASM • Viral - Coxsackie A and B, Influenza, adenovirus, HIV, etc. • Primary: mesothelioma, angiosarcoma • Bacterial - Staphylococcus, pneumococcus, TB, etc. • Metastatic – lung, breast, bone, lymphoma, melanoma • Fungal - Candida • Direct extension from adjoining tumor • Parasitic - Amoeba, candida, etc. • RADIATION PERICARDITIS • AUTOIMMUNE DISORDERS • RENAL FAILURE (uremia) • Systemic lupus erythematosus (SLE) • HYPOTHYROIDISM • Drug-Induced lupus (e.g. Hydralazine, Procainamide) • TRAUMATIC CARDIAC INJURY • Rheumatoid Arthritis • Penetrating - stab wound, bullet wound • Post Cardiac Injury Syndromes: • Blunt non-penetrating - automobile steering wheel accident • postmyocardial Infarction (Dressler's) Syndrome, postcardiotomy syndrome, etc. • IDIOPATHIC CLINICAL FEATURES: ACUTE PERICARDITIS • Chest pain : classic chest pain – sharp, pleuritic, is worse with supine position and improved on sitting upright, leaning forward. ( >85-90% of cases) • Pericardial Friction Rub ( <33% of cases) • EKG: Sinus tachycardia, diffuse ST elevation; PR segment depression; PR seg elevation in lead aVR. ( upto 60% of cases) • Additional symptoms: fever, leukocytosis, SIRS, cancer); elevated CRP, ESR; • Rarely elevation of troponins ( sign of myopericarditis) EKG FINDINGS IN ACUTE PERICARDITIS 4 Stages of ECG changes • Stage I • Diffuse ST elevation+PR depression(hrs to days) • Stage II • Normalization of ST/PR segments(days to weeks) • Stage III • Widespread T wave inversion(several weeks) • Stage IV • Gradual resolution of T wave inversions(months) DIAGNOSTIC TESTS • ECG is recommended in all patients. • Echocardiogram: Pericardial effusion • CXR is recommended in all patients • Blood tests : markers of inflammation- crp. And markers of myocardial injury ( troponin, CK) • Additional tests: if concern for other infections like TB. Serologic tests ( ANA, RF) to screen for connective tissue disease, screen for malignancy – lung, breast DIAGNOSIS/ TREATMENT: TREATMENT • Aspirin or NSAIDS are first line treatment of acute pericarditis. ( class I A) • Colchicine is recommended as first line adjunct treatment of acute pericarditis ( class I A) • Could check Sr CRP to assess therapy/guide treatment duration. ( class II ) • Exercise restriction – until pain resolves, CRP, ECG, Echo normalizes.; for athletes at least 3 mo. ( class II ) ; 6mo for myopericarditis (class I) • Corticosteroids are not recommended as first line therapy for acute pericarditis ( class III C) TREATMENT: PROGNOSIS: • Prognosis is generally good. • Bacterial/ TB pericarditis à high chances of developing constrictive pericarditis. • Patient who aren’t treated with colchicine à higher chances of developing recurrent pericarditis. • Recurrent pericarditis à may need addition of low dose steroids ( after excluding infection) ; for steroid dependent cases – consultation with rheum/ IVIG, anakinra, azathioprine may be considered. PERICARDIAL EFFUSION • Normal 15-50 ml of fluid • Common etiologies include: • Acute pericarditis • Autoimmune disease • Chest trauma • Malignancy-most often due to noncardiac primary tumors. • Mediastinal radiation • Renal failure with uremia • Aortic dissection extending into the pericardium • Certain drugs: Hydralazine, Minoxidil, Procainamide,INH • CHF, Cirrhosis, Hypothyroidism • Fluid composition: Serous, Fibrinous, Hemorrhagic, Purulent • Imaging: Echo, CT, MRI, +/-CXR PATHOPHYSIOLOGY • Symptoms of cardiac compression dependent on: • Volume of fluid • Rate of fluid accumulation • Compliance characteristics of the pericardium A. Sudden increase of small amount of fluid (e.g. trauma) B. Slow accumulation of large amount of fluid (e.g. CHF) CLINICAL FEATURES: • Small effusions do not produce hemodynamic Physical Findings: abnormalities. May be normal in patients without hemodynamic • Large effusions, in addition to causing compromise. hemodynamic compromise, may lead to When tamponade: compression of adjoining structures and produce symptoms of: • Muffled heart sounds • dysphagia (compression of esophagus) • Elevated JVP • • hoarseness (recurrent laryngeal nerve Rarely pericardial friction rub compression) • Pulsus paradoxus ( if tamponade) • hiccups (diaphragmatic stimulation) • Hypotension • dyspnea (pleural inflammation/effusion) • Fatigue, anorexia, cough, weakness, palpitations MECHANISM AND MEASUREMENT OF PULSUS PARADOXUS PERICARDIAL EFFUSION DIAGNOSTIC STUDIES “Water Bottle” Sign Electrical alternans CARDIAC TAMPONADE: ECHO • Chamber collapse • Dilated IVC • Respiratory flow variation of mitral and tricuspid velocities CARDIAC TAMPONADE ECHO FINDINGS IVC in Cardiac Tamponade CARDIAC TAMPONADE-ECHO FINDINGS CARDIAC TAMPONADE-ECHO FINDINGS CARDIAC TAMPONADE-ECHO FINDINGS Mitral Inflow in Cardiac Tamponade PERICARDIAL EFFUSION: LABS • Routine Labs: CMP, CBC, TFTs,ANA, screening for malignancy (age appropriate) • Echo: mainstay. Consider CT/ MRI if loculated, pericardial thickening, masses, chest abnormalities. • Diagnostic Pericardiocentesis yields diagnosis <40% of cases! • Fluid analysis : Cell count, protein, LDH, glucose, gram stain/CX, Cytology, AFB stain/Cx, PCR • PERICARDIAL EFFUSION: TREATMENT • Treatment: • With hemodynamic compromise: • Urgent pericardiocentesis – percutaneous or surgical • Treat underlying cause ( class I c) • Volume expansion – temporary • If associated with inflammation – consider ASA, NSAIDS, colchicine ( class I c) • Avoid diuresis. • Pericardiocentesis – to determine etiology • If hemodynamically stable: or for tamponade or if suspicion for • Monitor unknown bacterial or neoplastic etiology ( • Serial echo class Ic) • Treat underlying c • if reaccumulates – pericardial window/ if biopsy needed. PERICARDIOCENTESIS CONSTRICTIVE PERICARDITIS • Late complication of pericardial disease • Fibrous scar formation • Fusion of pericardial layers • Calcification further stiffens pericardium • A potentially curable entity in patients with heart failure with preserved ejection fraction but it is often underdiagnosed and missed. PATHOPHYSIOLOGY Scarred Pericardium Inhibits diastolic filling of both ventricles Venous Pressure Stroke Volume Pulmonary Cardiac Output JVP Congestion Hepatomegaly Ascites Peripheral Edema ETIOLOGY OF CONSTRICTIVE PERICARDITIS Developed Nations: Presenting Symptoms: Post pericarditis Volume Overload: Mediastinal Radiation - peripheral edema, Underdeveloped Nations & Immunocompromised: - anascara, • Tuberculosis - cardiac cirrhosis • Connective tissue disorder • Malignancy Diminshed Cardiac Output: • Trauma - Fatigue, • Uremic pericarditis. - Dypnea on exertion VENTRICULAR INTERDEPENDENCE CONSTRICTIVE PERICARDITIS- PHYSICAL FINDINGS • Elevated JVP • • Kussmaul’s Sign • Pericardial Knock • Pulsatile hepatomegaly • Pleural Effusion • Ascites • Peripheral Edema • Anascara DIAGNOSIS CXR: calcified cardiac silhouette CT or MRI: pericardial thickening CONSTRICTIVE PERICARDITIS . RIGHT HEART CATHETERIZATION Equalization of pressures- RV – LV discordance -Less than 5 mmHg, difference between mean RA, RV diastolic, PA diastolic, LV diastolic and pericardial pressures CONSTRICTION VS. RESTRICTION: TREATMENT • For chronic constrictive pericarditis- surgery is the treatment of choice. • Significant surgical mortality even in experienced centers(>6%) • Independent predictors of ↑mortality: • Older age • Higher NYHA class, • LVEF • PCWP • Worse renal failure • Lower serum Na • Certain etiologies From: Bertog, C. JACC 2004 SUMMARY • Acute pericarditis is most often of idiopathic or viral cause and is usually a self-limited illness. • Common clinical findings in acute pericarditis include pleuritic chest pain, fever, pericardial friction rub, and diffuse ST-segment elevation on the ECG, often accompanied by PR-segment depression. • Treatment of common acute pericarditis
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]
  • Common Arrhythmias Disclosures
    Common Arrhythmias Disclosures • I work for Virginia Garcia Memorial Health Center. • And I am a medical editor for Jones & Bartlett Publishing. Jon Tardiff, BS, PA-C OHSU Clinical Assistant Professor What a 12-Lead ECG can help you do • Diagnose ACS / AMI • Interpret arrhythmias • Identify life-threatening syndromes (WPW, LGL, Long QT synd., Wellens synd., etc) • Infer electrolyte imbalances • Infer hypertrophy of any chamber • Infer COPD, pericarditis, drug effects, and more! Arabic, Somali, Mai Mai, Pashtu, Urdu, ASL, and more! For example… WPW with Atrial Fib 55 66 Wolff-Parkinson-WhiteWPW Graphic synd. Same pt, converted to SR Drs. Wolff, Parkinson, & White 77 Another example: Dr. William Stokes—1800s 71 y.o. man with syncope This patient is conscious and alert! Third Degree Block 9 Treatment: permanent pacemaker 10 Lots of ways to read ECGs… Limitations of a 12-Lead ECG • QRSs wide or narrow? • Is it sinus rhythm or not? • Truly useful only ~40% of the time • Regular or irregular? • If not, is it atrial fibrillation? • Each ECG is only a 10 sec. snapshot • Fast or slow? • BBB? • P waves? • MI? • Serial ECGs are necessary, especially for ACS • Other labs help corroborate ECG findings (cardiac markers, Cx X-ray) • Confounders must be ruled out (LBBB, dissecting aneurysm, pericarditis, WPW, Symptoms: digoxin, LVH, RVH) • Syncope is bradycardia, heart blocks, or VT • Rapid heart beat is AF, SVT, or VT Conduction System Lead II P wave axis …upright in L II II R T P R U Q S …upright in L II R wave axis SA Node AV Node His Bundle BBs Purkinje Fibers 14 13 Q S Normal Sinus Rhythm Triplicate Method: 6-second strip: 6 seconds 300, 150, 100, Count PQRST cycles in a 6 75, 60, 50 second strip & multiply x 10 Quick, easy, sufficient Easy, & more accurate 300 150 100 75 60 6 seconds What is the heart rate? Horizontal axis is time (mS); vertical axis is electrical energy (mV) 16 1.
    [Show full text]
  • Comparison of Traditional and Plethysmographic Methods for Measuring Pulsus Paradoxus
    ARTICLE Comparison of Traditional and Plethysmographic Methods for Measuring Pulsus Paradoxus Jeff A. Clark, MD, FAAP; Mary Lieh-Lai, MD, FAAP; Ron Thomas, PhD; Kalyani Raghavan, MD; Ashok P. Sarnaik, MD, FAAP, FCCM Background: In the evaluation of patients with acute (PPpleth) on the pulse oximeter. Mean difference and asthma, pulsus paradoxus (PP) is an objective and non- 95% confidence intervals were calculated for each invasive indicator of the severity of airway obstruction. method. The 2 methods were also analyzed for correla- However, in children PP may be difficult or impossible tion and agreement using the Pearson product moment to measure. Indwelling arterial catheters facilitate the mea- correlation and a Bland and Altman plot. surement of PP, but they are invasive and generally re- served for critically ill patients. Results: Patients with status asthmaticus had higher PPausc and PPpleth readings compared with nonasthmatic pa- Objective: To determine the utility of the plethysmo- tients. Pulsus paradoxus measured by plethysmography graphic waveform (PPpleth) of the pulse oximeter in mea- in patients with and without asthma was similar to PPausc suring PP. readings (mean difference, 0.6 mm Hg; 95% confidence interval, −0.6 to 2.1 mm Hg). Individual PPpleth readings Methods: Patients from the pediatric intensive care showed significant correlation and agreement with PPausc unit, emergency department, and inpatient wards of a readings in patients both with and without asthma. tertiary care pediatric hospital were eligible for the study. A total of 36 patients (mean age [SD], 11.2 [4.7] Conclusion: Measurement of PP using the pulse oxim- years) were enrolled in the study.
    [Show full text]
  • Unstable Angina with Tachycardia: Clinical and Therapeutic Implications
    Unstable angina with tachycardia: Clinical and therapeutic implications We prospectively evaluated 19 patients with prolonged chest pain not evolving to myocardiai infarction and accompanied with reversible ST-T changes and tachycardia (heart rate >lOO beats/min) in order to correlate heart rate reduction with ischemic electrocardiographic (ECG) changes. Fourteen patients (74%) received previous long-term combined treatment with nifedipine and nitrates. Continuous ECG monitoring was carried out until heart rate reduction and at least one of the following occurred: (1) relief of pain or (2) resolution of ischemic ECG changes. The study protocol consisted of carotid massage in three patients (IS%), intravenous propranolol in seven patients (37%), slow intravenous amiodarone infusion in two patients (lo%), and intravenous verapamil in four patients (21%) with atrial fibrillation. In three patients (16%) we observed a spontaneous heart rate reduction on admission. Patients responded with heart rate reduction from a mean of 126 + 10.4 beats/min to 64 k 7.5 beats/min (p < 0.005) and an ST segment shift of 4.3 k 2.13 mm to 0.89 k 0.74 mm (p < 0.005) within a mean interval of 13.2 + 12.7 minutes. Fifteen (79%) had complete response and the other four (21%) had partial relief of pain. A significant direct correlation was observed for heart rate reduction and ST segment deviation (depression or elevation) (f = 0.7527 and 0.8739, respectively). These patients represent a unique subgroup of unstable angina, in which the mechanism responsible for ischemia is excessive increase in heart rate. Conventional vasodilator therapy may be deleterious, and heart rate reduction Is mandatory.
    [Show full text]
  • Pulsus Paradoxus
    ERJ Express. Published on December 6, 2012 as doi: 10.1183/09031936.00138912 Pulsus paradoxus Olfa Hamzaoui1, Xavier Monnet2,3, Jean‐Louis Teboul2,3 1. Hôpitaux Universitaires Paris‐Sud, Hôpital Antoine Béclère, Service de Réanimation Médicale, 157, rue de la Porte de Trivaux, 92141 Clamart, France. 2. Hôpitaux Universitaires Paris‐Sud, Hôpital de Bicêtre, service de réanimation médicale, 78, rue du Général Leclerc, Le Kremlin‐Bicêtre, F‐94270 France. 3. Université Paris‐Sud, Faculté de médecine Paris‐Sud, EA4533, Le Kremlin‐Bicêtre, 63, rue Gabriel Péri, F‐94270 France. Address for correspondence: Prof. Jean‐Louis Teboul Service de réanimation médicale Centre Hospitalier Universitaire de Bicêtre 78, rue du Général Leclerc 94 270 Le Kremlin‐Bicêtre France e‐mail: jean‐[email protected] Phone: + 33 1 45 21 35 47 Fax: + 33 1 45 21 35 51 1 Copyright 2012 by the European Respiratory Society. Abstract Systolic blood pressure normally falls during quiet inspiration in normal individuals. Pulsus paradoxus is defined as a fall of systolic blood pressure of more than 10 mmHg during the inspiratory phase. Pulsus paradoxus can be observed in cardiac tamponade and in conditions where intrathoracic pressure swings are exaggerated or the right ventricle is distended, such as severe acute asthma or exacerbations of chronic obstructive pulmonary disease. Both the inspiratory decrease in left ventricular stroke volume and the passive transmission to the arterial tree of the inspiratory decrease in intrathoracic pressure contribute to the occurrence of pulsus paradoxus. During cardiac tamponade and acute asthma, biventricular interdependence (series and parallel) plays an important role in the inspiratory decrease in left ventricular stroke volume.
    [Show full text]
  • Respiration Driven Excessive Sinus Tachycardia Treated with Clonidine Matthew Emile Li Kam Wa,1 Patricia Taraborrelli,1 Sajad Hayat,2 Phang Boon Lim1
    Novel treatment (new drug/intervention; established drug/procedure in new situation) BMJ Case Reports: first published as 10.1136/bcr-2016-216818 on 28 April 2017. Downloaded from CASE REPORT Respiration driven excessive sinus tachycardia treated with clonidine Matthew Emile Li Kam Wa,1 Patricia Taraborrelli,1 Sajad Hayat,2 Phang Boon Lim1 1Department of Cardiology, SUMMARY no evidence of dual AV node physiology, accessory Imperial College Healthcare A 26-year-old man presented to our syncope service pathway or inducible supraventricular tachycardia. NHS Trust, London, UK 2Department of Cardiology, with debilitating daily palpitations, shortness of breath, A subsequent permanent pacemaker led to no University Hospitals Coventry presyncope and syncope following a severe viral further episodes of frank syncope. However his and Warwickshire NHS Trust, respiratory illness 4 years previously. Mobitz type II block ongoing debilitating exertional and respiratory- Coventry, UK had previously been identified, leading to a permanent driven palpitations with presyncope remained. pacemaker and no further episodes of frank syncope. Conservative measures including increased fluid Correspondence to Dr Phang Boon Lim, Transthoracic echocardiography, electophysiological study intake and compression stockings had no effect. [email protected] and repeated urine metanepherines were normal. His Trials of medication including fludrocortisone, fle- palpitations and presyncope were reproducible on deep cainide, β blockers and ivabradine were either not Accepted 18 December 2016 inspiration, coughing, isometric hand exercise and tolerated or had no significant effect on his passive leg raises. We demonstrated rapid increases in symptoms. heart rate with no change in morphology on his 12 lead During a simple active stand over 3 min, his ECG.
    [Show full text]
  • Basic Rhythm Recognition
    Electrocardiographic Interpretation Basic Rhythm Recognition William Brady, MD Department of Emergency Medicine Cardiac Rhythms Anatomy of a Rhythm Strip A Review of the Electrical System Intrinsic Pacemakers Cells These cells have property known as “Automaticity”— means they can spontaneously depolarize. Sinus Node Primary pacemaker Fires at a rate of 60-100 bpm AV Junction Fires at a rate of 40-60 bpm Ventricular (Purkinje Fibers) Less than 40 bpm What’s Normal P Wave Atrial Depolarization PR Interval (Normal 0.12-0.20) Beginning of the P to onset of QRS QRS Ventricular Depolarization QRS Interval (Normal <0.10) Period (or length of time) it takes for the ventricles to depolarize The Key to Success… …A systematic approach! Rate Rhythm P Waves PR Interval P and QRS Correlation QRS Rate Pacemaker A rather ill patient……… Very apparent inferolateral STEMI……with less apparent complete heart block RATE . Fast vs Slow . QRS Width Narrow QRS Wide QRS Narrow QRS Wide QRS Tachycardia Tachycardia Bradycardia Bradycardia Regular Irregular Regular Irregular Sinus Brady Idioventricular A-Fib / Flutter Bradycardia w/ BBB Sinus Tach A-Fib VT PVT Junctional 2 AVB / II PSVT A-Flutter SVT aberrant A-Fib 1 AVB 3 AVB A-Flutter MAT 2 AVB / I or II PAT PAT 3 AVB ST PAC / PVC Stability Hypotension / hypoperfusion Altered mental status Chest pain – Coronary ischemic Dyspnea – Pulmonary edema Sinus Rhythm Sinus Rhythm P Wave PR Interval QRS Rate Rhythm Pacemaker Comment . Before . Constant, . Rate 60-100 . Regular . SA Node Upright in each QRS regular . Interval =/< leads I, II, . Look . Interval .12- .10 & III alike .20 Conduction Image reference: Cardionetics/ http://www.cardionetics.com/docs/healthcr/ecg/arrhy/0100_bd.htm Sinus Pause A delay of activation within the atria for a period between 1.7 and 3 seconds A palpitation is likely to be felt by the patient as the sinus beat following the pause may be a heavy beat.
    [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]
  • Cardiac Tamponade Management Clinical Guideline
    Cardiac Tamponade Management Clinical Guideline V1.0 August 2020 Summary Cardiac Tamponade Management Clinical Guideline V1.0 Page 2 of 20 1. Introduction 1.1 Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid, blood, pus, clots or gas in the pericardial space, resulting in reduced ventricular filling and subsequent haemodynamic compromise. This includes a haemodynamic spectrum ranging from incipient or preclinical tamponade (when pericardial pressure equals right atrial pressure but it is lower than left atrial pressure) to haemodynamic shock with significant reduction of stroke volume and blood pressure, the latter representing a life-threatening medical emergency. 1.2 The diagnosis of cardiac tamponade is essentially a clinical diagnosis requiring echocardiographic confirmation of the initial diagnostic suspicion. In most patients, cardiac tamponade should be diagnosed by clinical examination that typically shows elevated systemic venous pressure, tachycardia, muffled heart sounds and paradoxical arterial pulse. Systemic blood pressure may be normal, decreased, or even elevated. Clinical signs may also include decreased electrocardiographic voltage with electrical alternans and an enlarged cardiac silhouette on chest X-ray with slow-accumulating effusions. 1.3 Once a clinical diagnosis of tamponade is suspected, an echocardiogram should be performed without delay. The diagnosis is then confirmed by echocardiographic demonstration of several 2D and Doppler-based findings (i.e. evidence of pericardial effusion with variable cardiac chambers’ compression, abnormal respiratory variation in tricuspid and mitral valve flow velocities, inferior vena cava plethora). 1.4 This should immediately trigger On-call Consultant Cardiologist review in order to stratify the patient risk, identify specific supportive and monitoring requirements and guide the optimal timing and modality of pericardial drainage.
    [Show full text]
  • Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives
    Basic Cardiac Rhythms – Identification and Response Module 1 ANATOMY, PHYSIOLOGY, & ELECTRICAL CONDUCTION Objectives ▪ Describe the normal cardiac anatomy and physiology and normal electrical conduction through the heart. ▪ Identify and relate waveforms to the cardiac cycle. Cardiac Anatomy ▪ 2 upper chambers ▪ Right and left atria ▪ 2 lower chambers ▪ Right and left ventricle ▪ 2 Atrioventricular valves (Mitral & Tricuspid) ▪ Open with ventricular diastole ▪ Close with ventricular systole ▪ 2 Semilunar Valves (Aortic & Pulmonic) ▪ Open with ventricular systole ▪ Open with ventricular diastole The Cardiovascular System ▪ Pulmonary Circulation ▪ Unoxygenated – right side of the heart ▪ Systemic Circulation ▪ Oxygenated – left side of the heart Anatomy Coronary Arteries How The Heart Works Anatomy Coronary Arteries ▪ 2 major vessels of the coronary circulation ▪ Left main coronary artery ▪ Left anterior descending and circumflex branches ▪ Right main coronary artery ▪ The left and right coronary arteries originate at the base of the aorta from openings called the coronary ostia behind the aortic valve leaflets. Physiology Blood Flow Unoxygenated blood flows from inferior and superior vena cava Right Atrium Tricuspid Valve Right Ventricle Pulmonic Valve Lungs Through Pulmonary system Physiology Blood Flow Oxygenated blood flows from the pulmonary veins Left Atrium Mitral Valve Left Ventricle Aortic Valve Systemic Circulation ▪ Blood Flow Through The Heart ▪ Cardiology Rap Physiology ▪ Cardiac cycle ▪ Represents the actual time sequence between
    [Show full text]
  • Acute Non-Specific Pericarditis R
    Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from Postgrad. med. J. (August 1967) 43, 534-538. CURRENT SURVEY Acute non-specific pericarditis R. G. GOLD * M.B., B.S., M.RA.C.P., M.R.C.P. Senior Registrar, Cardiac Department, Brompton Hospital, London, S.W.3 Incidence neck, to either flank and frequently through to the Acute non-specific pericarditis (acute benign back. Occasionally pain is experienced on swallow- pericarditis; acute idiopathic pericarditis) has been ing (McGuire et al., 1954) and this was the pre- recognized for over 100 years (Christian, 1951). In senting symptom in one of our own patients. Mild 1942 Barnes & Burchell described fourteen cases attacks of premonitory chest pain may occur up to of the condition and since then several series of 4 weeks before the main onset of symptoms cases have been published (Krook, 1954; Scherl, (Martin, 1966). Malaise is very common, and is 1956; Swan, 1960; Martin, 1966; Logue & often severe and accompanied by listlessness and Wendkos, 1948). depression. The latter symptom is especially com- Until recently Swan's (1960) series of fourteen mon in patients suffering multiple relapses or patients was the largest collection of cases in this prolonged attacks, but is only partly related to the country. In 1966 Martin was able to collect most length of the illness and fluctuates markedly from of his nineteen cases within 1 year in a 550-bed day to day with the patient's general condition. hospital. The disease is thus by no means rare and Tachycardia occurs in almost every patient at warrants greater attention than has previously some stage of the illness.
    [Show full text]
  • Recurrent Takotsubo Cardiomyopathy: a Rare Diagnosis with a Common Emergency Department Presentation Emily M Miner, Harini Gurram, Tennie Renkens and Julie L
    Case Report iMedPub Journals ARCHIVES OF MEDICINE 2017 http://www.imedpub.com/ Vol.9 No.4:8 ISSN 1989-5216 DOI: 10.21767/1989-5216.1000229 Recurrent Takotsubo Cardiomyopathy: A Rare Diagnosis with a Common Emergency Department Presentation Emily M Miner, Harini Gurram, Tennie Renkens and Julie L. Welch* Department of Emergency Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA *Corresponding author: Julie L Welch, Department of Emergency Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA, Tel: 317-962-8880; E-mail: [email protected] Received date: August 08, 2017; Accepted date: August 14, 2017; Published date: August 16, 2017 Citation: Miner EM, Gurram H, Renkens T, Welch JL. Recurrent Takotsubo Cardiomyopathy: A Rare Diagnosis with a Common Emergency Department Presentation. Arch Med. 2017, 9:4 Copyright: © 2017 Miner EM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The incidence of recurrent Takotsubo cardiomyopathy after initial diagnosis is about 5% at 6 years with recurrence being Abstract more common when the initial episode has more severe left ventricular dysfunction [4]. While the long-term prognosis of Takotsubo cardiomyopathy is a non-ischemic Takotsubo is favorable in >95% of cases, acute symptoms of an cardiomyopathy that is often triggered by a physical or episode can be life-threatening and lead to cardiogenic shock emotional stressor and commonly affects post-menopausal [5]. Proper diagnosis is crucial in these life-threatening women. A 57 year old female with a significant past medical history for atrial fibrillation, anxiety, and Takotsubo situations.
    [Show full text]