Bedside clues to the diagnosis of heart disease

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  • Bedside Clues to the Diagnosis of

    Heart Disease*

    JOHN F. GOODWIN, M.D .

    London, England

    A

    PARTof bedside diagnosis, the modern

    cardiologist is entitled to an electrocardio-

    gram and good chest x-ray film in order to make

    a clinical assessment of cardiovascular disease .

    In this lecture I shall hope to show how, on

    the basis of the personal experience of myself and

    of my colleagues at the Postgraduate Medical

    School of London, bedside clues have helped to

    arrive at a final diagnosis in certain forms of

    congenital and acquired disease . Naturally,

    such a lecture can touch only superficially on a

    few disorders, but it is hoped that what I have to

    say will be of some value in indicating the impor-

    tant principles of diagnosis at the bedside . In

    particular, I should like to stress that clinical

    bedside diagnosis is essential in planning the

    type of investigation needed to arrive at a final

    and comprehensive picture of the patient's illness .

    JUGULAR VENOUS PULSE

    I shall begin by considering the jugular venous

    pressure, to the study of which the late Paul

    Wood brought so much fruitful endeavor .' It

    should be realized that this pulse has much to

    tell the physician before the external jugular

    veins become distended . Jugular venous dis-

    tension is often merely a sign of mediastinal

    obstruction or gross elevation of jugular venous

    pressure . The aim should be to recognize the

    normal jugular venous pulse, and its abnormal

    characteristics in various forms of disease at a

    stage when pulsation of the deep veins only can

    he seen and there may be no filling of the ex-

    ternal jugular veins .

    The normal venous pressure should just he visible

    to a height of I to 3 cm. above the sternal angle

    with the patient lying at 45 .

    A normal venous pulse consists of three main

    waves, the a wave due to atrial contraction,

    which is followed by a negative or x wave due to

    atrial relaxation .' This is followed by a second

    positive deflection, the v wave due to atrial filling

    and obstruction to blood flow during ventricular

    systole, which in turn is succeeded by a negative

    deflection, the y wave, which is due to emptying

    of the atrium as the tricuspid valve opens and

    the blood enters the ventricle . There is some-

    times a small positive deflection on the down-

    stroke of the x wave, the c wave, which may be

    due to ventricular contraction and tricuspid

    valve closure, but often, at least on external

    jugular phlebographic records, is due to carotid

    artefact .

    Figure 1 shows a very crude and purely

    diagrammatic representation of the jugular

    venous pulses and the auscultatory phenomena

    in four heart diseases which affect the jugular

    venous pulse in a distinctive way . This diagram

    is not to scale.2

    Pulmonary Hypertension : The upper of the

    four diagrams represents the jugular venous

    pulse in pulmonary hypertension . As a result

    of the right ventricular hypertension, right atrial

    hypertrophy occurs, and this produces an aug-

    mented a wave in the jugular venous pulse,

    which can be seen as a flicking pulsation above

    the sternal angle lateral to the carotid pulse and

    preceeding it . In cases of extreme right atrial

    hypertrophy, the a wave may be palpable .

    The auscultatory phenomena in severe pul-

    monary hypertension consist of a short ejection

    systolic murmur, which is often soft, preceded

    by a pulmonary ejection click . The pulmonary

    component of the second heart sound is always

    accentuated and narrowly separated from aortic

    closure . There may be a fourth heart sound

    due to atrial hypertrophy and corresponding to

    the a wave, and occasionally a soft high pitched

    * From the Postgraduate Medical School and Hammersmith Hospital, London, England .

    Guest Lecture read at the 13th Annual Meeting of the American College of Cardiology, New Orleans, February 16,

    1964.

    VOLUME 15, JANUARY 1965 81

  • 82

    FVLMOEMRY

    MYDERTENION

    (SEVERE

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    ~TENOOP

    sEVERE

    TRICVSEID

    STENOS/5

    CARDIAC

    CONSTRICTION

    JVOVLAR

    VENCELt NLSE

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    (LEFTSYERNALEoRSit

    FIG . 1 . Schematic representation of the jugular uenour pulse and

    auscultatory signs in pulmonary hypertension, lone pulmo-

    nary stenosis, tricuspid stenosis and cardiac constric-

    tion . (The drawings are not to scale .) (A = atrial

    sound . I = first heart sound . C = systolic c lick . SM =

    systolic murmur. A, = aortic valve closure . P, =

    pulmonary valve closure . PDM = pulmonary dia-

    stolic murmur . TSM = tricuspid systolic murmur .

    TMDM = tricuspid mid-diastolic murmur) . See text

    for description of jugular venous pulse waves . (Repro-

    duced from Clinical Disorders ofthe Pulmonary Circula-

    don by permission of the publishers . J. & A . Churchill

    Ltd.%).

    early diastolic murmur is heard at the left sternal

    edge, due to pulmonary valvar incompetence .

    Pulmonary Stenosis :Although the jugular

    venous pulse in pulmonary stenosis with closed

    ventricular septum differs in no way from that of

    pulmonary hypertension, because the cause is

    the same, the auscultatory phenomena are en-

    tirely different . The systolic murmur is of a

    diamond shape, maximal in mid- and late

    systole, extremely loud and accompanied by a

    thrill . The murmur extends over the sound

    made by aortic closure up to the soft and de-

    layed pulmonary closure . In both conditions

    the right ventricle is large and may be felt as a

    tapping substernal impulse or sometimes may

    lift the sternum when dilatation is added to

    hypertrophy. When tricuspid incompetence

    occurs as a complication, the x descent of the

    Goodwin

    jugular venous pulse is obliterated and replaced

    by a large systolic wave due to regurgitation of

    blood from the ventricle into the atrium during

    ventricular systole .

    Tricuspid Stenosis : In this condition, de-

    picted in the third diagram, the a wave is also

    augmented, but the y descent due to atrial

    emptying, instead of being sharp, is slow and

    leisurely, reflecting the obstruction to inflow to

    the ventricle . There is commonly an atrial

    sound, and since tricuspid incompetence may

    accompany tricuspid stenosis, there may be a

    systolic murmur in the tricuspid area . Usually,

    there is a low-pitched rumbling diastolic mur-

    mur heard in the same area, increasing on in-

    spiration .

    Cardiac Constriction : Finally, when the heart

    is constricted by constrictive pericarditis, peri-

    cardial effusion or by endomyocardial disease,

    the a and v waves are augmented, and x and y

    descents sharp, the y descent being particularly

    obvious . The a and v waves reflect the high

    ventricular end-diastolic pressure which causes

    an increased right atrial pressure ; the sharp x

    descent indicates the absence of tricuspid in-

    competence while the y descent reflects rapid

    filling of the ventricle due to absence of tricuspid

    valve obstruction . The murmurs in cardiac

    constriction are often trivial, as shown in the

    diagram, the second sound being commonly

    widely split, and there is nearly always a third

    sound which coincides in time with the end-

    diastolic pressure in the right ventricle and with

    the y descent . The third sound is due to the

    sudden arrest of ventricular filling by the thick

    pericardium . The cardiac impulse reveals a

    diastolic thrust coinciding with the early dia-

    stolic sound . 8

    Thus, by attention to the jugular venous pulse

    and auscultation, considerable information of

    great value may be obtained at the bedside in

    elucidating these four groups of disorder .

    There are, of course, many other abnormalities

    of thejugular venous pulse . These have merely

    been selected to illustrate the value of appreciat-

    ing the form of the venous pulse .

    PULMONARY HYPERTENSION

    Returning to pulmonary hypertension, it must

    be noted that there are many causes and degrees

    of severity. The physical signs which have

    been mentioned represent extreme pulmonary

    hypertension such as is met with in conditions in

    which the pulmonary vascular bed at arteriolar

    level is obliterated by extreme vasoconstriction

    THE AMERICAN JOURNAL OF CARDIOLOGY

  • or obliterative disease such as thromboembolism .

    The facies in such pulmonary hypertension may

    be characteristic, consisting of bright red cheeks,

    with marked circumoral pallor . The color of

    the cheeks differs slightly from the characteristic

    mitral facies in that the color tends to be red or

    scarlet rather than purple, but the difference on

    occasions may only be slight . These facies are

    not usually seen in patients with milder forms of

    pulmonary hypertension such as that due to

    excessive pulmonary blood flow or moderate

    vasoconstriction .

    The cause of pulmonary hypertension may often be

    substantially elucidated at the bedside . One of

    the commonest causes is a left-sided cardiac

    lesion which produces pulmonary venous hyper-

    tension, which in turn excites pulmonary ar-

    teriolar vasoconstricti