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Central Venous Pressure Venous Examination but Underestimates Ultrasound Accurately Reflects the Jugular
Ultrasound Accurately Reflects the Jugular Venous Examination but Underestimates Central Venous Pressure Gur Raj Deol, Nicole Collett, Andrew Ashby and Gregory A. Schmidt Chest 2011;139;95-100; Prepublished online August 26, 2010; DOI 10.1378/chest.10-1301 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/139/1/95.full.html Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright2011by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692 Downloaded from chestjournal.chestpubs.org at UCSF Library & CKM on January 21, 2011 © 2011 American College of Chest Physicians CHEST Original Research CRITICAL CARE Ultrasound Accurately Refl ects the Jugular Venous Examination but Underestimates Central Venous Pressure Gur Raj Deol , MD ; Nicole Collett , MD ; Andrew Ashby , MD ; and Gregory A. Schmidt , MD , FCCP Background: Bedside ultrasound examination could be used to assess jugular venous pressure (JVP), and thus central venous pressure (CVP), more reliably than clinical examination. Methods: The study was a prospective, blinded evaluation comparing physical examination of external jugular venous pressure (JVPEXT), internal jugular venous pressure (JVPINT), and ultrasound collapse pressure (UCP) with CVP measured using an indwelling catheter. We com- pared the examination of the external and internal JVP with each other and with the UCP and CVP. -
Practical Cardiac Auscultation
LWW/CCNQ LWWJ306-08 March 7, 2007 23:32 Char Count= Crit Care Nurs Q Vol. 30, No. 2, pp. 166–180 Copyright c 2007 Wolters Kluwer Health | Lippincott Williams & Wilkins Practical Cardiac Auscultation Daniel M. Shindler, MD, FACC This article focuses on the practical use of the stethoscope. The art of the cardiac physical exam- ination includes skillful auscultation. The article provides the author’s personal approach to the patient for the purpose of best hearing, recognizing, and interpreting heart sounds and murmurs. It should be used as a brief introduction to the art of auscultation. This article also attempts to illustrate heart sounds and murmurs by using words and letters to phonate the sounds, and by presenting practical clinical examples where auscultation clearly influences cardiac diagnosis and treatment. The clinical sections attempt to go beyond what is available in standard textbooks by providing information and stethoscope techniques that are valuable and useful at the bedside. Key words: auscultation, murmur, stethoscope HIS article focuses on the practical use mastered at the bedside. This article also at- T of the stethoscope. The art of the cardiac tempts to illustrate heart sounds and mur- physical examination includes skillful auscul- murs by using words and letters to phonate tation. Even in an era of advanced easily avail- the sounds, and by presenting practical clin- able technological bedside diagnostic tech- ical examples where auscultation clearly in- niques such as echocardiography, there is still fluences cardiac diagnosis and treatment. We an important role for the hands-on approach begin by discussing proper stethoscope selec- to the patient for the purpose of evaluat- tion and use. -
Bates' Pocket Guide to Physical Examination and History Taking
Lynn S. Bickley, MD, FACP Clinical Professor of Internal Medicine School of Medicine University of New Mexico Albuquerque, New Mexico Peter G. Szilagyi, MD, MPH Professor of Pediatrics Chief, Division of General Pediatrics University of Rochester School of Medicine and Dentistry Rochester, New York Acquisitions Editor: Elizabeth Nieginski/Susan Rhyner Product Manager: Annette Ferran Editorial Assistant: Ashley Fischer Design Coordinator: Joan Wendt Art Director, Illustration: Brett MacNaughton Manufacturing Coordinator: Karin Duffield Indexer: Angie Allen Prepress Vendor: Aptara, Inc. 7th Edition Copyright © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins. Copyright © 2009 by Wolters Kluwer Health | Lippincott Williams & Wilkins. Copyright © 2007, 2004, 2000 by Lippincott Williams & Wilkins. Copyright © 1995, 1991 by J. B. Lippincott Company. All rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appear- ing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins at Two Commerce Square, 2001 Market Street, Philadelphia PA 19103, via email at [email protected] or via website at lww.com (products and services). 9 8 7 6 5 4 3 2 1 Printed in China Library of Congress Cataloging-in-Publication Data Bickley, Lynn S. Bates’ pocket guide to physical examination and history taking / Lynn S. -
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. -
Scoliosis, Alters the Position of the Beat
Br Heart J: first published as 10.1136/hrt.8.3.162 on 1 July 1946. Downloaded from THE HEART IN STERNAL DEPRESSION BY WILLIAM EVANS From the Cardiac Department ofthe London Hospital Received June 25, 1946 The place where the apex beat appears on the chest wall depends as much on the symmetry of the thorax as on the size of the heart. A change in the alignment of the spine, the posterior fulcrum of the thoracic cage, in the form of scoliosis, alters the position of the beat. Local deformity of the ribs which form the walls of the cage will do the same thing. Deformity of the sternum, the anterior fulcrum of the thorax, as a cause of displacement of the apex beat has received less attention. The effects of depression of the sternum (pectus excavatum) on the shape and position of the heart have been studied in sixteen adults examined during the past year. DESCRIPTION OF CASES All sixteen patients had been referred for an explanation of certain signs connected with the heart, with the knowledge that deformity of the chest was present, but without appreciating that the two conditions might be related. In many of them suspicion of heart disease had led to restriction of their physical activities and to a change of design for their future livelihood. The symptoms that had caused the patients to seek medical advice in the first place were http://heart.bmj.com/ TABLE I SUMMARY OF FINDNGS IN 16 HEALTHY SUBJECTS WITH DEPRESSED STERNUM Antero-posterior Radiological findings in anterior view chest measurement _ _ Case Age Sternal in inches No. -
5 Precordial Pulsations
Chapter 5 / Precordial Pulsations 113 5 Precordial Pulsations CONTENTS MECHANICS AND PHYSIOLOGY OF THE NORMAL APICAL IMPULSE PHYSICAL PRINCIPLES GOVERNING THE FORMATION OF THE APICAL IMPULSE NORMAL APICAL IMPULSE AND ITS DETERMINANTS ASSESSMENT OF THE APICAL IMPULSE LEFT PARASTERNAL AND STERNAL MOVEMENTS RIGHT PARASTERNAL MOVEMENT PULSATIONS OVER THE CLAVICULAR HEADS PULSATIONS OVER THE SECOND AND/OR THIRD LEFT INTERCOSTAL SPACES SUBXIPHOID IMPULSE PRACTICAL POINTS IN THE CLINICAL ASSESSMENT OF PRECORDIAL PULSATIONS REFERENCES In this chapter the pulsations of the precordium will be discussed in relation to their identification, the mechanisms of their origin, and their pathophysiological and clinical significance. Precordial pulsations include the “apical impulse,” left parasternal movement, right parasternal movement, pulsations of the clavicular heads, pulsations over the second left intercostal space, and subxiphoid impulses. MECHANICS AND PHYSIOLOGY OF THE NORMAL APICAL IMPULSE Since during systole the heart contracts, becoming smaller and therefore moving away from the chest wall, why should one feel a systolic outward movement (the apical impulse) at all? Logically speaking there should not be an apical impulse. Several different methods of recording the precordial motion have been used to study the apical impulse going back to the late 19th century (1,2). Among the more modern methods, the notable ones are the recordings of the apexcardiogram (3–17), the impulse cardiogram (18), and the kinetocardiogram (19–21). While apexcardiography records the relative displacement of the chest wall under the transducer pickup device, which is often held by the examiner’s hands, the proponents of the impulse cardiography and kinetocardiography point out that these methods allow the recording of the absolute movement of the chest wall because the pickup device is anchored to a fixed point held 113 114 Cardiac Physical Examination in space away from the chest. -
Topic: MITRAL HEART DISEASES: BASIC SYMPTOMS and SYNDROMES on the BASIS of CLINICAL and INSTRUMENTAL METHODS of EXAMINATION
Topic: MITRAL HEART DISEASES: BASIC SYMPTOMS AND SYNDROMES ON THE BASIS OF CLINICAL AND INSTRUMENTAL METHODS OF EXAMINATION 1. What hemodynamic changes cause complaints of patients with mitral stenosis for cough, shortness of breath, hemoptysis? A. reduction of systemic blood pressure; B. increased pressure in the small circulatory system; C. stagnation of blood in the liver; D. enlargement of the left atrium and contraction of the mediastinum; E. Reduction of blood flow from the left ventricle. 2. What complaints are caused by a decrease in minute volume of blood in patients with mitral stenosis? A) cough, shortness of breath, hemoptysis; C) fever, joint pain, general weakness; C) heartache, heart failure, palpitations; D) lower extremity swelling, heaviness in the right hypochondrium; E) headache, dizziness, general weakness, fatigue. 3. Data palpation of the heart area with mitral stenosis: A) no change is observed; B) apex beat displaced to the left, resistant; C) apex beat weakened or undetectable; D) there is an increased pulsation in the second intercostal space to the left; E) there is a systolic "cat murmur" in the second intercostal space to the right. 4. What forced position can occupy a patient with mitral stenosis? A) knee-elbow; B) a Bedouin who prays; C) orthopnoe; D) opistotonus; E) outside the pointing dog 5. What does the face of a patient with mitral stenosis look like? A) swollen, cyanotic; B) swollen, pale, enophthalmos observed; C) the face of a "wax doll"; D) swollen, pale, with swelling under and above the eyes; E) pale, with cyanotic blush, cyanosis of the tip of the nose, ear lobes, chin. -
Jugular Venous Pressure
NURSING Jugular Venous Pressure: Measuring PRACTICE & SKILL What is Measuring Jugular Venous Pressure? Measuring jugular venous pressure (JVP) is a noninvasive physical examination technique used to indirectly measure central venous pressure(i.e., the pressure of the blood in the superior and inferior vena cava close to the right atrium). It is a part of a complete cardiovascular assessment. (For more information on cardiovascular assessment in adults, see Nursing Practice & Skill ... Physical Assessment: Performing a Cardiovascular Assessment in Adults ) › What: Measuring JVP is a screening mechanism to identify abnormalities in venous return, blood volume, and right heart hemodynamics › How: JVP is determined by measuring the vertical distance between the sternal angle and the highest point of the visible venous pulsation in the internal jugular vein orthe height of the column of blood in the external jugular vein › Where: JVP can be measured in inpatient, outpatient, and residential settings › Who: Nurses, nurse practitioners, physician assistants, and treating clinicians can measure JVP as part of a complete cardiovascular assessment What is the Desired Outcome of Measuring Jugular Venous Pressure? › The desired outcome of measuring JVP is to establish the patient’s JVP within the normal range or for abnormal JVP to be identified so that appropriate treatment may be initiated. Patients’ level of activity should not be affected by having had the JVP measured ICD-9 Why is Measuring Jugular Venous Pressure Important? 89.62 › The JVP is -
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 -
Clinical Assessment in Acute Heart Failure
Hellenic J Cardiol 2015; 56: 285-301 Review Article Clinical Assessment in Acute Heart Failure 1 2 NIKOLAOS S. KAKOUROS , STAVROS N. KAKOUROS 1University of Massachusetts, MA, USA; 2Cardiac Department, “Amalia Fleming” General Hospital, Athens, Greece Key words: eart failure (HF) is defined as “a clear precipitant or trigger. It is very im Heart failure, complex clinical syn drome that portant to establish the precipitating diagnosis, physical examination, H can result from any structural or causes, which may have therapeutic and congestion. functional cardiac disorder that impairs the prognostic implications. Approximate ability of the ventricle to fill with, or eject ly 60% of patients with AHF have doc blood.” HF has an estimated overall prev umented CAD. Myocardial ischemia in alence of 2.6%. It is becoming more com the setting of acute coronary syndromes mon in adults older than 65 years, because is a precipitant or cause, particularly in of increased survival after acute myocar patients presenting with de novo AHF.4 dial infarction (AMI) and improved treat AHF is also often precipitated by medica ment of coronary artery disease (CAD), tion and dietary noncompliance, as well val vular heart disease and hypertension.1 as by many other conditions, which are Acute HF (AHF) is an increasingly com summarized in Table 1. Once the diagno mon cause of hospitalizations and mortality sis of AHF is confirmed, initial therapy in worldwide. In the majority of patients, AHF cludes removal of precipitants; if this can Manuscript received: can be attributed to worsening chronic HF, be carried out successfully, the patient’s August 25, 2014; and approximately 4050% of this group have subsequent course may be stable. -
Table 1 -- Signs That Suggest Heart Failure
TABLES FOR HEART FAILURE CLINICAL PROCESS GUIDELINES Table 1 -- Signs That Suggest Heart Failure Tachycardia Third heart sound (S3) Increased jugular venous pressure Positive hepatojugular reflux Bilateral rales Peripheral edema not due to venous insufficiency Laterally displaced apical impulse Weight gain AMDA Heart Failure Clinical Practice Guideline 2002 Table 2 -- Symptoms That Suggest Heart Failure Dyspnea on exertion Dyspnea at rest Orthopnea Paroxysmal nocturnal dyspnea Fatigue Decreased exercise tolerance Unexplained cough, especially at night Acute confusional state, delirium Abdominal symptoms (nausea, abdominal pain or distention) Decreased food intake Decline in functional status AMDA Heart Failure Clinical Practice Guideline 2002 Table 3 -- Risk Factors for Heart Failure Coronary artery disease (angina or myocardial infarction) Chronic hypertension Idiopathic dilated cardiomyopathy Valvular heart disease (e.g., mitral regurgitation, aortic stenosis) Other cardiomyopathy (e.g., sarcoidosis) Arrhythmia (e.g., sarcoidosis) Anemia Fluid volume overload with noncardiac causes Thyroid disease (hypo- or hyperthyroidism) AMDA Heart Failure Clinical Practice Guideline 2002 Table 4 -- New York Association Functional Classification Class I -- No limitations of physical activity. No shortness of breath, fatigue, or heart palpitations with ordinary physical activity. Class II -- Slight limitation of physical activity. Shortness of breath, fatigue, or heart palpitations with ordinary physical activity, but patients are comfortable at rest. -
The Jugular Venous Pressure Revisited
REVIEW CME EDUCATIONAL OBJECTIVE: Readers will measure and interpret the jugular venous pressure in their patients CREDIT with heart failure JOHN MICHAEL S. CHUA CHIACO, MD NISHA I. PARIKH, MD, MPH DAVID J. FERGUSSON, MD Cardiovascular Disease, John A. Burns School Assistant Professor, John A. Burns School Clinical Professor of Medicine, Department of Medicine, University of Hawaii, Honolulu of Medicine, University of Hawaii; of Cardiology, John A. Burns School The Queen’s Medical Center, Honolulu of Medicine, University of Hawaii; The Queen’s Medical Center, Honolulu The jugular venous pressure revisited ■■ ABSTRACT n this age of technological marvels, I it is easy to become so reliant on them as Assessment of the jugular venous pressure is often inad- to neglect the value of bedside physical signs. equately performed and undervalued. Here, we review Yet these signs provide information that adds the physiologic and anatomic basis for the jugular venous no cost, is immediately available, and can be pressure, including the discrepancy between right atrial repeated at will. and central venous pressures. We also describe the cor- Few physical findings are as useful but as rect method of evaluating this clinical finding and review undervalued as is the estimation of the jugular the clinical relevance of the jugular venous pressure, venous pressure. Unfortunately, many practi- especially its value in assessing the severity and response tioners at many levels of seniority and experi- to treatment of congestive heart failure. Waveforms ence do not measure it correctly, leading to a vicious circle of unreliable information, lack reflective of specific conditions are also discussed.