DOCSLIB.ORG

The Physiologic Mechanisms of Cardiac and Vascular Physical Signs

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Physiologic Mechanisms of Cardiac and Vascular Physical Signs 184 J AM cou. CARDIOl 1983:1:184-98 The Physiologic Mechanisms of Cardiac and Vascular Physical Signs JOSEPH K. PERLOFF, MD, FACC Los Angeles. California Examination of the heart and circulation includes five relate cardiac and vascular physicalsigns to their mech• items: 1) the patient's physical appearance, 2) the ar• anisms, focusing on each of the five sources. It draws terial pulse, 3) the jugular venous pulse and peripheral liberally on early accounts, emphasizing that modern veins, 4) the movements of the heart-observation, pal• investigative techniques often serve chiefly to verify hy• pation and percussion of the precordium, and 5) aus• potheses posed in the past. cultation. This report deals with specific examples that I shall begin by acknowledging three debts. The first is to chain of events, has provided answers to many of the re• the late Paul Wood and his staff at the Institute of Car• maining questions (2,3). diology , London, where my under standing of the physio• Let us now tum to specific examples that relate cardiac logic meaning of cardiac and vascular physical signs began. and vascular physical signs to their mechanisms, focusin g The second debt is to the Fulbright Foundation and the on each of the five sources mentioned. In so doing, certain Institute for International Education for making my year in illustrative examples will be selected. No attempt will be England possible. The third debt is to the National Institutes made to be comprehensive. of Health for providing my first research grant , which sup• ported the continuation of these studies in the United States. That grant was approved exactl y 25 years ago , the year The Physical Appearance during which the first issue of the official journal of the Cyanosis and clubbing of the digits serve as useful points American College of Cardiology was published. of departure. Differential cyanosis and clubbing exist when Examination of the heart and circulation focuses on five these signs are present in the feet but not in the hands, and items: I) the patient's physical appearance, 2) the arterial reflect a right to left shunt through a patent ductus arteriosus pulse , 3) the jugular venous pulse and peripheral veins, 4) with intact ventricular septum (4). The physiologic mech• the movements of the heart-observation, palpation and anism requires that pulmonary vascular resistance exceed percu ssion of the precordium, and 5) auscultation (I). The systemic resistance so that unoxygenated blood from the pul• chain of events that has culminated in our present under• monary trunk flows through the ductus into the aorta just standing of the physiologic mechanisms of the physical signs distal to the left subclavian artery (Fig. I); the toes are began with bedside observations by a host of brilliant cli• cyanosed and clubbed selectively. In another form of dif• nicians; their descriptions of specific signs stand today as ferential cyanosis-designated by convention " reversed models of clarity. Then followed the graphic record that differential cyano sis" - the opposite is true. The toes are allowed more refined analysis of the arterial pulse, the jug• less cyanotic and clubbed than the fingers (4). This dis• ular venous pulse , precordial movement and heart sounds tinctive physical appearance also has a relatively precise and murmurs. The next major step , the cardiac catheter. pathoph ysiologic basis-the aorta is right ventricular in or• permitted hemodynamic, angiographic and intracardiac igin (cyanotic hands), while the pulmonary trunk is either phonocardiographic observations not previousl y possible . right ventricular or biventricular in origin, arising just above Echocard iograph y. the most recent advance in this exciting a ventricular septal defect so that oxygenated blood from the left ventricle enters the pulmonary trunk . In the presence of high pulmonary vascular resistance. this oxygenated blood From the Divisions of Cardiology, Departments of Medicine and Pe• flows through a patent ductu s arteriosus into the descending diatrics, UCLA Center for the Health Sciences. Los Angeles, California. Address for reprints: Joseph K. Perloff, MD. UCLA Center for the aorta and to the lower limbs (relatively acyanotic feet) (4). Health Sciences, Room 47-123. Los Angeles. California 90024. Thus. sophisticated diagnoses are based on nothing more © 1983 by the American College of Cardiol ogy 0735-1097/83/010184-15$03.00 MECHANISMS OF CARDIOVASCULAR PHYSICAL SIGNS J AM Call CARDIOl 185 1983;1:184-98 Righ'·'....." .hun' Desc Ao a b than comparison of the physical appearances of upper and Figure 1. (a) Schematic illustration of the mechanism of differential cy• lower limbs. anosis and clubbing. Unoxygenated blood from the pulmonary trunk (PT) flows through the patent ductus arteriosus (PDA) and enters the aorta (Ao) distal to the left subclavian artery (LSA). (b) A catheter takes this course in a 13 year old girl with reversed flow through a large ductus. Desc Ao The Arterial Pulse = descending aorta. Analysis of waveform. This is one of the most im• portant aspects of the examination of the arterial pulse. In (I) drew a careful distinction between pulsus bigeminus and severe valvular aortic stenosis (Fig. 2), the arterial pulse is pulsus altemans, the latter a term that Traube introduced. diminished (small) with a slow ascending limb (parvus), He wrote, "The following case...demonstrates a variation but in addition, the peak is illdefined and late (tardus) (5). of the pulsus bigerninus: I designated it the name of 'pulsus Mackenzie (6) understood the physiologic mechanism, writ• altemans'. .It involves a succession of high and low ing, "When there is marked narrowing of the aortic orifice, pulses, in such a manner that a low pulse regularly the full effect of the ventricular systole upon the arterial follows a high pulse...." Traube's report included a pho• column is not at once developed, as the aortic stenosis offers tograph of typical beat to beat alternans recorded with Mar• an increased resistance. Hence, the impact of the pulse wave ey's sphygmograph applied to the radial artery. The mech• on the finger is not sudden, but feels to push against the anism of pulsus bigeminus is clear enough (simple fixed finger in a somewhat leisurely fashion. The tracing in such coupling as in digitalis toxicity). Pulsus alternans is one a case represents a slanting of the stroke with an interruption reflection of depressed left ventricular function, but the pre• near the top-an anacrotic-pulse tracing." cise mechanism of the beat to beat alternation in rate of rise Characteristics of arterial pulse. A strong arterial pulse and peak pressure remains elusive. occurs either with or without increased pulse pressure, the Differential pulsations. With regard to differential pul• latter epitomized by the visible Corrigan's pulse of chronic sations, coarctation of the aorta epitomizes the relation be• free aortic regurgitation (7). An increasedarterialpulse (strong, tween simple physical signs and their anatomic and phys• hyperkinetic) with normal pulse pressure is a feature of iologic mechanisms (4). Important variations in the anatomic chronic severe mitral regurgitation, for example (small water• location of the coarctation can be inferred from bedside hammer pulse) because the left ventricle ejects at a high analysis of the arterial pulse. Equal and brisk brachial and velocity while the diastolic pressure in the aortic root re• carotid pulses with absent or diminished femoral pulses mains normal (8). Similarly, high velocity left ventricular place the coarctation distal to the left subclavian artery. ejection accounts for the brisk arterial pulse with normal When right and left brachial arterial pulses are compared, pulse pressure in hypertrophic obstructive cardiomyopathy. an absent or relatively small left brachial pulse means that Pulsus bigeminus and alternans. Ludwig Traube (1872) the coarctation compromises the orifice of the left subclavian 186 J AM cou, CARDIOl PERlOFF 1983:1:184--98 P QRS Figure 2. (a) Apexeardiogram showing mid-dia• stolic and presystolic distension (arrows) of the left ventricle in a patient with valvular aortic ste• nosis and heart failure. (b) Left ventricular (LV) pressure pulse with identical configuration (ar• rows ). The brachial artery pulse (BA) shows the typical slow rate of rise and sustained peak of severe aortic stenosis. a artery . Absence or diminution of the right brachial pulse stantly finds clinical evidence of the ready occurrence of implies anomalous origin ofthe right subclavian artery distal tricuspid incompetence in the study of the venous pulse." to the coarctation. In supravalvular aortic stenosis , differ• A tall V wave with a rapid Y descent implies that the ential pulsations take the form of an increase in pulse pres• tricuspid orifice is unobstructed . Conversely, a tall V wave sure and rate of rise of right brachial and carotid pulses. with an inappropriately slow, gentle Y descent is a feature The zone of supravalvular stenosis directs a high velocity of obstruction at the tricuspid orifice, typically rheumatic jet into the innominate artery, disproportionately increasing tricuspid stenosis with atrial fibrillation (10). Despite a tall the systolic pressure in the right carotid and subclavian V crest , the Y descent is slow because the stenotic tricuspid arteries (4,5). In addition, the Coanda effect (affinity of a orifice puts an effective break on the rate of right ventricular jet stream to adhere to a wall) carries the high velocity jet filling in the presence of a high right atrial pressure . into the orifice of the innominate artery (4). Constrictive pericarditis. The jugular venous pulse in constrictive pericarditis is distinctive, and its mechanism is clear (13). The A and V waves are high and equal yet The Jugular Venous Pulse inconspicious because the marked elevation of mean right Giant A waves. In 1867, Potain not only accurately atrial pressure puts the crests above the angle of the jaw described the normal waveform of the internal jugular vein, (Fig.
Load more

Recommended publications
  • 4.17-Kronzon-M-Mode-Echo.Pdf
    M-Mode Echocardiography Is it still Alive? Itzhak Kronzon, MD,FASE Honoraria: Philips Classical M-mode Echocardiography M-Mode offers better time and image resolution. Sampling Rate M-Mode: 1800 / sec 2D: 30 / sec Disadvantages 1. Single Dimension (depth only) 2. Nonperpendicular orientation (always use 2D guidance). Normal MV MS M-Mode of RA & LA Myxomas Back cover of ECHOCARDIOGRAPHY Feigenbaum, 3rd edition MV Prolapse M-Mode in HOCM ASH / SAM Mid-systolic AV Closure Markers of LV Dysfunction A-C Shoulder (“B-Bump”) EPSS Feigenbaum, ECHOCARDIOGRAPHY What does the m-mode show? 1. MS 2. AI 3. Flail MV 4. Myxoma Answer: 3. Posterior Leaflet Motion in Flail MV Note that the posterior leaflet moves anteriorly in early diastole, before it moves posteriorly. ASD with Large L to R Shunt Note markedly dilated RV and “paradoxical” septal motion Dyssynchrony by M-Mode -LBBB 138msec Dyssynchrony of >130msec is associated with good CRT response (sensitivity 100%, specificity 63%) This M mode finding is not associated with increased risk of A. Coarctation B. Pulmonic Stenosis C. Subaortic Stenosis D. Aortic insufficiency Echo of pt with Endocarditis and Shock Best Rx is: 1. AVR 2. MVR 3. IABP 4. Can not tell Echo of pt with Endocarditis and Shock Answer: 1. AVR Note premature closure of MV & echogenic mass in LVOT (Ao veg. Vs. flail Ao cusp) Differential Dx of Premature MV Closure A. AR B. First Degree AV Block C. High Degree AV Block D. Blocked APC E. Atrial Flutter The most likely physical finding in this pt is 1. Absent left subclavian pulse 2.
    [Show full text]
  • Heart Murmurs
    HEART MURMURS PART I BY WILLIAM EVANS From the Cardiac Department of the London Hospital Received November 5, 1946 Auscultation of the heart, depending as it does on the acuity of the auditory sense and providing information commensurate with the observer's experience, cannot always determine unequivocally the various sound effects that may take place during systole and diastole. It is not surprising, therefore, that auscultation tied to traditional theories may sometimes lead to a wrong interpretation of the condition, although a judgment born of ripe experience in clinical medicine and pathology will avoid serious mistakes. It is more than fortuitous that modern auscultation has grown on such a secure foundation, but it is imperative that for the solution of outstanding problems there should be precise means of registering heart sounds. This is why a phonocardiogram was included in the examination of a series of patients pre- senting murmurs. As each patient attended for the test, the signs elicited on clinical auscultation were first noted and an opinion was formed on their significance. Cardioscopy was invariably carried out, and, when necessary, teleradiograms were taken. Limb and chest lead electrocardiograms were frequently recorded in addition to the lead selected as a control for the phonocardiogram. Many cases came to necropsy. The simultaneous electrocardiogram and sound record was taken by a double string galvanometer supplied by the Cambridge Instrument Company, and the length of the connecting tube leading from the chest to the amplifier was 46 cm. Although the amplitude of sounds and murmurs was matched against each other in individual patients, there was no attempt to standardize the intensity of murmurs in terms of amplitude in different patients; in fact it was varied deliberately in order to produce such excursion of the recording fibre as would best show the murmur.
    [Show full text]
  • Does This Patient Have Aortic Regurgitation?
    THE RATIONAL CLINICAL EXAMINATION Does This Patient Have Aortic Regurgitation? Niteesh K. Choudhry, MD Objective To review evidence as to the precision and accuracy of clinical examina- Edward E. Etchells, MD, MSc tion for aortic regurgitation (AR). Methods We conducted a structured MEDLINE search of English-language articles CLINICAL SCENARIO (January 1966-July 1997), manually reviewed all reference lists of potentially relevant You are asked to see a 59-year-old articles, and contacted authors of relevant studies for additional information. Each study woman with liver cirrhosis who will be (n = 16) was independently reviewed by both authors and graded for methodological undergoing sclerotherapy for esopha- quality. geal varices. When she was examined by Results Most studies assessed cardiologists as examiners. Cardiologists’ precision for her primary care physician, she had a detecting diastolic murmurs was moderate using audiotapes (k = 0.51) and was good pulse pressure of 70 mm Hg. The pri- in the clinical setting (simple agreement, 94%). The most useful finding for ruling in mary care physician is concerned about AR is the presence of an early diastolic murmur (positive likelihood ratio [LR], 8.8- the possibility of aortic regurgitation 32.0 [95% confidence interval {CI}, 2.8-32 to 16-63] for detecting mild or greater AR (AR) and asks you whether endocardi- and 4.0-8.3 [95% CI, 2.5-6.9 to 6.2-11] for detecting moderate or greater AR) (2 tis prophylaxis is necessary for sclero- grade A studies). The most useful finding for ruling out AR is the absence of early di- astolic murmur (negative LR, 0.2-0.3 [95% CI, 0.1-0.3 to 0.2-0.4) for mild or greater therapy.
    [Show full text]
  • Case Reports
    Case Reports Quadrivalvular Heart Disease An Autopsied Case with Massive Pulmonary Regurgitation Tsuguya SAKAMOTO, M.D., Zen'ichiro UOZUMI, M.D., Nobuyoshi KAWAI, M.D., Yoshiyuki SAKAMOTO, M.D., Ryoko KATO, M.D., and Hideo UEDA, M.D. SUMMARY An autopsied case of quadrivalvular heart disease was described, in which pulmonary regurgitation due to possible bicuspid valve was pre- dominant and tricuspid stenosis, mitral stenosis, and aortic stenosis with insufficiency coexisted. The patient was 47, and finally 53 years old female with long-term history of cough due to bronchial compression by the enormously dilated pulmonary artery. Clinical examination revealed massive pulmonary regurgitation, which was further substantiated by right heart catheterization and cineangiocardiography. The phono- cardiograms and the reference tracings suggested the co-existence of tricuspid stenosis, aortic stenosis with regurgitation and mitral stenosis. Cardiac catheterization, intracardiac phonocardiography and angio- cardiography also favored to the diagnosis of organic tricuspid stenosis. However, the ignorance of the presence of such an unusual combination misled to the precise antemortem diagnosis. Discussion was made on the rarity of quadrivalvular heart disease, and the pathogenesis of this unusual pulmonary regurgitation was analyzed based on the autopsy finding and the history as well as the clinical mani- festation. Finally, combination of the murmurs of organic and relative tricuspid stenosis was presented to explain the acoustical findings of the present case. Additional Indexing Words: Phonocardiography Mechanocardiography Bronchial compression Right-sided Austin Flint murmur UADRIVALVULAR heart disease was first described by Shattuck1) in 1891. However, the involvement of all four valves in a given patient is extremely rare.2) The present paper describes one of such case, in which From the Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Tokyo.
    [Show full text]
  • Viding Diagnostic Insights Into the Pathophysiologic Mechanisms
    viding diagnostic insights into the pathophysiologic mechanisms under- lying the acoustic findings heard in clinical practice.162-165 Contemporary physicians should take advantage of the valuable clinical information that can be obtained by such an inexpensive instrument and expedient and reli- able tool as the stethoscope. The following section reviews the funda- mental technique of cardiac auscultation, emphasizing the diagnostic value and practical clinical applications of this time-honored (but endan- gered) art in this time of need.166 The Art and Technique of Cardiac Auscultation. Auscultation of the heart and vascular system is one of the most challenging and rewarding clinical diagnostic skills that can (and should) be learned and applied by every prac- ticing physician. Proficiency in cardiac auscultation requires experience, repeated practice, and a great deal of patience (and patients). Most impor- tantly, it requires a proper state of mind. (“we hear what we listen for”). Although the most vital component of the auscultatory apparatus lies between the earpieces, the proper use of a well-designed, efficient stetho- scope cannot be overemphasized. To ensure optimal sound transmission, the well-crafted stethoscope should be airtight, with snug but comfortably-fit- ting earpieces, properly aligned metal binaurals, and flexible, double-barrel, 1 thick-walled tubing, ⁄8 inch in internal diameter and no more than 12 to 15 inches in length. A high-quality stethoscope should be equipped with both bell and diaphragm chest pieces. The bell, when applied gently to the skin, will “bring out” low frequency sounds and murmurs (eg, faint S4 or S3 gal- lop or diastolic rumble) and the diaphragm, when pressed firmly against the skin, will accentuate high-pitched acoustic events (eg, diastolic blowing murmur of AR).
    [Show full text]
  • 4B. the Heart (Cor) 1
    Henry Gray (1821–1865). Anatomy of the Human Body. 1918. 4b. The Heart (Cor) 1 The heart is a hollow muscular organ of a somewhat conical form; it lies between the lungs in the middle mediastinum and is enclosed in the pericardium (Fig. 490). It is placed obliquely in the chest behind the body of the sternum and adjoining parts of the rib cartilages, and projects farther into the left than into the right half of the thoracic cavity, so that about one-third of it is situated on the right and two-thirds on the left of the median plane. Size.—The heart, in the adult, measures about 12 cm. in length, 8 to 9 cm. in breadth at the 2 broadest part, and 6 cm. in thickness. Its weight, in the male, varies from 280 to 340 grams; in the female, from 230 to 280 grams. The heart continues to increase in weight and size up to an advanced period of life; this increase is more marked in men than in women. Component Parts.—As has already been stated (page 497), the heart is subdivided by 3 septa into right and left halves, and a constriction subdivides each half of the organ into two cavities, the upper cavity being called the atrium, the lower the ventricle. The heart therefore consists of four chambers, viz., right and left atria, and right and left ventricles. The division of the heart into four cavities is indicated on its surface by grooves. The atria 4 are separated from the ventricles by the coronary sulcus (auriculoventricular groove); this contains the trunks of the nutrient vessels of the heart, and is deficient in front, where it is crossed by the root of the pulmonary artery.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • ACC/AAP/AHA/ASE/HRS/SCAI/SCCT/SCMR/SOPE 2014 Appropriate Use Criteria for Initial Transthoracic Echocardiography in Outpatient P
    JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY VOL. - ,NO.- ,2014 ª 2014 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 0735-1097/$36.00 PUBLISHED BY ELSEVIER INC. http://dx.doi.org/10.1016/j.jacc.2014.08.003 1 APPROPRIATE USE CRITERIA 55 2 56 3 57 4 ACC/AAP/AHA/ASE/HRS/ 58 5 59 6 SCAI/SCCT/SCMR/SOPE 60 7 61 8 2014 Appropriate Use Criteria for 62 9 63 10 Initial Transthoracic Echocardiography 64 11 65 12 in Outpatient Pediatric Cardiology 66 13 67 14 A Report of the American College of Cardiology Appropriate Use Criteria Task Force, 68 15 American Academy of Pediatrics, American Heart Association, American Society of 69 16 Echocardiography, Heart Rhythm Society, Society for Cardiovascular Angiography and 70 17 Interventions, Society of Cardiovascular Computed Tomography, Society for Cardiovascular 71 18 Magnetic Resonance, and Society of Pediatric Echocardiography 72 19 73 20 74 21 75 22 76 Q1 Writing Group for Robert M. Campbell, MD, FACC, FAHA, FAAP, FHRS, Wyman W. Lai, MD, MPH, FACC, FASE 23 77 Echocardiography Chair Leo Lopez, MD, FACC, FAAP, FASE 24 78 in Outpatient Ritu Sachdeva, MD, FACC, FAAP, FASE 25 79 Pediatric Pamela S. Douglas, MD, MACC, FAHA, FASE 26 80 Cardiology Benjamin W. Eidem, MD, FACC, FASE 27 81 28 82 29 83 30 Rating Panel Robert M. Campbell, MD, FACC, FAHA, FAAP, FHRS, Richard Lockwood, MD** 84 yy 31 Chair* G. Paul Matherne, MD, MBA, FACC, FAHA 85 zz 32 Pamela S. Douglas, MD, MACC, FAHA, FASE, Moderator* David Nykanen, MD, FACC 86 yy 33 Catherine L.
    [Show full text]
  • Anatomy of the Heart
    Anatomy of the Heart DR. SAEED VOHRA DR. SANAA AL-SHAARAWI OBJECTIVES • At the end of the lecture, the student should be able to : • Describe the shape of heart regarding : apex, base, sternocostal and diaphragmatic surfaces. • Describe the interior of heart chambers : right atrium, right ventricle, left atrium and left ventricle. • List the orifices of the heart : • Right atrioventricular (Tricuspid) orifice. • Pulmonary orifice. • Left atrioventricular (Mitral) orifice. • Aortic orifice. • Describe the innervation of the heart • Briefly describe the conduction system of the Heart The Heart • It lies in the middle mediastinum. • It is surrounded by a fibroserous sac called pericardium which is differentiated into an outer fibrous layer (Fibrous pericardium) & inner serous sac (Serous pericardium). • The Heart is somewhat pyramidal in shape, having: • Apex • Sterno-costal (anterior surface) • Base (posterior surface). • Diaphragmatic (inferior surface) • It consists of 4 chambers, 2 atria (right& left) & 2 ventricles (right& left) Apex of the heart • Directed downwards, forwards and to the left. • It is formed by the left ventricle. • Lies at the level of left 5th intercostal space 3.5 inch from midline. Note that the base of the heart is called the base because the heart is pyramid shaped; the base lies opposite the apex. The heart does not rest on its base; it rests on its diaphragmatic (inferior) surface Sterno-costal (anterior)surface • Divided by coronary (atrio- This surface is formed mainly ventricular) groove into : by the right atrium and the right . Atrial part, formed mainly by ventricle right atrium. Ventricular part , the right 2/3 is formed by right ventricle, while the left l1/3 is formed by left ventricle.
    [Show full text]
  • 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
    [Show full text]
  • The Functional Anatomy of the Heart. Development of the Heart, Anomalies
    The functional anatomy of the heart. Development of the heart, anomalies Anatomy and Clinical Anatomy Department Anastasia Bendelic Plan: Cardiovascular system – general information Heart – functional anatomy Development of the heart Abnormalities of the heart Examination in a living person Cardiovascular system Cardiovascular system (also known as vascular system, or circulatory system) consists of: 1. heart; 2. blood vessels (arteries, veins, capillaries); 3. lymphatic vessels. Blood vessels Arteries are blood vessels that carry blood away from the heart. Veins carry blood back towards the heart. Capillaries are tiny blood vessels, that connect arteries to veins. Lymphatic vessels: lymphatic capillaries; lymphatic vessels (superficial and deep lymph vessels); lymphatic trunks (jugular, subclavian, bronchomediastinal, lumbar, intestinal trunks); lymphatic ducts (thoracic duct and right lymphatic duct). Lymphatic vessels Microcirculation Microcirculatory bed comprises 7 components: 1. arterioles; 2. precapillaries or precapillary arterioles; 3. capillaries; 4. postcapillaries or postcapillary venules; 5. venules; 6. lymphatic capillaries; 7. interstitial component. Microcirculation The heart Heart is shaped as a pyramid with: an apex (directed downward, forward and to the left); a base (facing upward, backward and to the right). There are four surfaces of the heart: sternocostal (anterior) surface; diaphragmatic (inferior) surface; right pulmonary surface; left pulmonary surface. External surface of the heart The heart The heart has four chambers: right and left atria; right and left ventricles. Externally, the atria are demarcated from the ventricles by coronary sulcus (L. sulcus coronarius). The right and left ventricles are demarcated from each other by anterior and posterior interventricular sulci (L. sulci interventriculares anterior et posterior). Chambers of the heart The atria The atria are thin-walled chambers, that receive blood from the veins and pump it into the ventricles.
    [Show full text]