Cardiac Physical Examination

7/28/2019 Cardiac Physical Examination

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Bayu Laksono

Kartika Kristianto

Gloria Tanjung

Cardiac Physical Examination


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A. Inspeksi jantung

Tanda-tanda yang diamati :

(1) bentuk prekordium

(2) Denyut pada apeks jantung

(3) Denyut nadi pada dada

(4) Denyut vena


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bentuk prekordium

Pada umumnya kedua belah dada adalah simetris

Prekordium yang cekung dapat terjadi akibat

perikarditis menahun, fibrosis atau atelektasis

paru, scoliosis atau kifoskoliosis

Prekordium yang gembung dapat terjadi akibat daripembesaran jantung, efusi epikardium, efusi

pleura, tumor paru, tumor mediastinum


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sternotomy pada garis tengah menunjukkanbypass sebelumnya, torakotomi lateral

menunjukkan operasi bypass minimal invasif (left

internal mammary artery to left anterior

descending coronary artery) atau katup mitralsebelumnya


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Denyut apeks jantung (iktus kordis)

Dalam keadaaan normal, dengan sikap duduk, tidur terlentangatau berdiri iktus terlihat didalam ruangan interkostal V sisi kiriagak medial dari linea midclavicularis sinistra

Pada anak-anak iktus tampak pada ruang interkostal IV

Sifat iktus :

Pada keadaan normal, iktus hanya merupakan tonjolan kecil, yangsifatnya local. Pada pembesaran yang sangat pada bilik kiri, iktusakan meluas.

Iktus hanya terjadi selama systole.Oleh karena itu, untuk memeriksaiktus, kita adakan juga palpasi pada a. carotis comunis untukmerasakan adanya gelombang yang asalnya dari systole.


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Denyutan nadiApabila di dada bagian atas terdapat denyutan

maka harus curiga adanya kelainan pada aorta

Aneurisma aorta ascenden dapat menimbulkandenyutan di ruang interkostal II kanan,

sedangkan denyutan dada di daerah ruanginterkostal II kiri menunjukkan adanya dilatasi a.pulmonalis dan aneurisma aorta descenden


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Carotid pulse Diperiksa amplitudo, kontur, variasi, waktu carotid

upstroke berhubung S1 dan S2

Penyebab menurun pulsasi termasuk penurunan

stroke volume dan faktor di arteri seperti penyempitan

atherosclerotic atau penyumbatan Pulsus alternans, bigeminal pulse (beat-to-beat

variation); paradoxical pulse (respiratory variation)

Delayed carotid upstroke in aorticstenosis


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Denyutan vena

Vena yang tampak pada dada dan punggungtidak menunjukkan denyutan

Vena yang menunjukkan denyutan hanyalah

vena jugularis interna dan eksterna


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JVP

Peningkatan tekanan menandakan CHF,constrictive pericarditis, tricuspid stenosis, or SVC

obstruction

98% spesifik untuk peningkatan ventrikel kiri dan

rendahnya fraksi ejeksi ventrikel kiri dan ini

meningkatkan resiko kematian dari gagal jantung


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Palpasi jantung

Urutan palpasi dalam rangka pemeriksaanjantung adalah sebagai berikut :

Pemeriksaan iktus cordis

Pemeriksaan getaran / thrill

Pemeriksaan gerakan trachea


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Pemeriksaan iktus cordis

Hal yang dinilai adalah lokasi, diameter, terabatidaknya iktus, dan apabila teraba dinilai kuat

angkat atau tidak, dan durasi.

Kadang-kadang kita tidak dapat melihat, tetapi

dapat meraba iktus

Pada keadaan normal iktus cordis dapat teraba

pada ruang interkostal kiri V, agak ke medial (2

cm) dari linea midklavikularis kiri.


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The apical impulse may be displaced upward andto the left by pregnancy or a high left diaphragm.

Lateral displacement from cardiac enlargement in

congestive heart failure, cardiomyopathy,

ischemic heart disease. Displacement in

deformities of the thorax and mediastinal shift.


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Pemeriksaan getaran / thrill Adanya getaran seringkali menunjukkan adanya

kelainan katub bawaan atau penyakit jantungcongenital.

Disini harus diperhatikan : Lokalisasi dari getaran

Terjadinya getaran : saat systole atau diastole

Getaran yang lemah akan lebih mudah dipalpasi apabilaorang tersebut melakukan pekerjaan fisik karena frekuensi

jantung dan darah akan mengalir lebih cepat.

Dengan terabanya getaran maka pada auskultasi nantinya

akan terdengar bising jantung


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Thrills dapat menyertai keras, keras, ataugemuruh murmur sebagai pada stenosis aorta,

patent ductus arteriosus, defek septum ventrikel,

dan stenosis, mitral


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Pemeriksaan gerakan trachea

Pada pemeriksaan jantung, trachea harus jugadiperhatikan karena anatomi trachea

berhubungan dengan arkus aorta

Pada aneurisma aorta denyutan aorta menjalar

ke trachea dan denyutan ini dapat teraba


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Pemeriksaan arteri perifer Palpate the radial pulse with the pads of your fingers on the

flexor surface of the wrist laterally. Partially flexing the patients

wrist may help you feel this pulse. Compare the pulses in both

arms.

-Prominent veins in an edematous arm suggest venous

obstruction brachial pulse. Flex the patients elbow slightly, and with the

thumb of your opposite hand palpate the artery just medial to the

biceps tendon at the antecubital crease

- check arterial insuffieciency


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femoral feel at the midinguinal point (midway between thesymphysis pubis and the anterior superior iliac spine, just inferior

to the inguinal ligament)

popliteal feel deep in the center of the popliteal fossa with thepatient lying on their back with their knees bent

- widened femoral and popliteal pulse suggests an aneurysm of

the popliteal artery. Neither popliteal nor femoral aneurysms are

common. They are usually due to atherosclerosis, and occur

primarily in men over age 50.


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posterior tibial feel behind the medial malleolus

dorsalis pedis feel over the second metatarsalbone just lateral to the extensor hallucis tendon


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The dorsalis pedis artery may be congenitally absent or maybranch higher in the ankle. Search for a pulse more laterally.

Decreased or absent foot pulses (assuming a warm

environment) with normal femoral and popliteal pulses suggest

occlusive disease in the lower popliteal artery or its branches a

pattern often associated with diabetes mellitus. Sudden arterial occlusion, as by embolism or thrombosis, causes

pain and numbness or tingling. The limb distal to the occlusion

becomes cold, pale, and pulseless. Emergency treatment is

required. If collateral circulation is good, only numbness and

coolness may result.


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Percussion


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Percussion

Careful percussion will usually reveal

whether the heart is normal in size or

whether it is definitely marked

enlarged.

One should use the lightest percussion

possible and, with experience, rely

more and more upon the vibratory


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To determine the left border of the heart,percussion should begin at the lateral side and

percuss toward the sternum. The dullness usually

reveal along mid clavicular line.


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To determine the left border of the heart percussfrom left lateral toward medial.

The left border : the anterior axillary line.

The right border : the right sternal line.

the upper border (base of the heart): 2nd left

interspace.


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Physiologic changes in the area of

cardiac dullness

The position of the heart, and with it the area ofcardiac dullness, is influenced by the level of the

diaphragm.

In deep inspiration the diaphragm descends,producing a decrease in cardiac dullness, while in

forced expiration the diaphragm rises and produces

an increase in the cardiac dullness.


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In the later months of pregnancy thediaphragm is pushed upward, causing the

heart to lie more horizontally and closer to the

chest wall, thus increasing the area of cardiac

dullness.


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Cardiac dullness in

abdominal distention

A variety of pathologic conditions such asascites, an ovarian cyst, or peritonitis may

cause an elevation of the diaphragm with an

increase in the area of cardiac dullness.


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Changes in position of

cardiac dullness

A left-sided pleural effusion will push the heart

to the right, and increase the cardiac dullness

to the right of sternum, the left border in suchcases can usually not be made out. A right-

sided pleural effusion increase the cardiac

dullness on left side.


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In pneumothorax the heart is displaced toward

the normal side, but in massive collapse of the

lung the heart is displaced toward the affected

side.

Pleural adhesions may pull the heart to the

affected side with resulting changes in

cardiac dullness similar to those produced bycollapse of the lung.


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Decrease in the area of

cardiac dullness

A decrease in the relative cardiacdullness may occur in pulmonary

emphysema. The absolute cardiac

dullness is usually decreased insuch cases, since the lung is

increased in size and covers a

greater area of the heart than

normal.


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Increase in the area of

cardiac dullness

An increase in the area of cardiac dullness is

most strikingly seen in patients with cardiac

disease. we cannot detect by percussion an

appreciable increase of the cardiac dullness inhypertrophy of the heart unless there is an

accompanying dilatation.


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Cardiac enlargement

Enlargement of the left ventricle produces anincrease in the relative cardiac dullness to the

left and often downward on this side.

The heart silhouette looks like a shoe


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Enlargement of the left ventricle appears inaortic insufficiency, in aortic stenosis, in mitral

insufficiency, in longstanding hypertension

and in chronic nephritis. It is called aortic

heart.

Right ventricular enlargement, the cardiac

dullness will extended to left and upward. Ifthe right ventricular is severely enlarged, the

right border of the heart will extend to the right.

It is seen in cor pulmonale, in mitral stenosis,

in tricuspid insufficiency etc.


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Both the left atrium and pulmonary arteryenlarged, the pulmonary artery will be

exaggerated to leftward. The cardiac

silhouette is like a pear and called mitral heart,

it is frequently seen in mitral valve stenosis.

The heart silhouette is like a

ear


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Aortic dilation, aneurysm of aorta, pericardialeffusion, all those diseases may cause thebase border of heart enlargement, so that thebase border of the heart will be widened.

Congestive heart failure, severe myocarditis,Keshan disease, dilated myocardiopathy maycause the heart silhouette extending both to

right and left.


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Pericardial effusion

The cardiac dullness is increased in alldirections and assumes the form of a triangle

with the apex at the level of the first or second

intercostal space or a general globular

enlargement.

The heart silhouette is like

a flask

The heart silhouette is like a globe


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Adhesive pericarditis

The degree of enlargementdepends on the extent of the

adhesive process. The relative, and

especially the absolute, cardiacdullness are both markedly

increased to left and to the right.


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Increase in the absolute

cardiac dullness

Increase in the absolute cardiac dullnesswithout demonstrable cardiac enlargement

occurs when the left lung is retracted and a

larger area of the ventricle is exposed.

It also occurs in mediastinal tumors when the

heart is pushed up against the chest wall and

a large area of the ventricle comes into directcontact with the anterior surface of the chest.


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AUSCULTATION


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First Heart Sounds S1 is produced by closure of the mitral and tricuspid

valves in early systole

is loudest near the apex of the heart

it is high-frequency sound best heard with

diaphragm of stethoscope

mitral closure usually precedes tricuspid closure

they are separated by only about 0.01 sec

so,, human ear appreciates only a single sound

if right bundle branch is blocked mitral &

tricuspid may be audible split due to delayed

closure of tricuspid valve

F d i h i i f


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Factor determinate the intensity of

S1

the distance separating the leaflets of the openvalves at the onset ventricular contraction

relates to PR interval

the mobility of the leaflets (normal or rigid due to

stenosis)

the rate of rise of ventricular pressure


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Altered Intensity of S1

accentuated S1 shortened PR interval

mild mitral stenosis

high cardiac output states or tachycardia (eg.

exercise or anemia)

diminished S1

lengthened PR interval: first-degree AV nodal block

mitral regurgitation

severe mitral stenosis

stiff left ventricle (eg. systemic hypertension)


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Second Heart Sounds S2 results from the closure of the SL valves has 2 components:

aortic (A2)

pulmonic (P2)

Components of S2 are heard varying sounds with

respiratory cycle: (this situation is termed normal

or physiologic splitting)

theyre normally fused as one sound during

expiration

theyre audibly separated during inspiration


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during inspiration expansion of the chest intrathoracic pressure more negative

capacitance ( impedance) of the intrathoracic

pulmonary vessels temporary delay in the

diastolic backpressure of the pulmonary artery P2 is delayed (occurs later during inspiration

than during expiration)


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Abnormalities of S2

alteration of its intensity changes in the pattern of splitting


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Alterations of its intensity of S2

Depends on: velocity of blood coursing back toward the valves

from the aorta and pulmonary artery after the

completion of ventricular contraction

the suddenness with which that motion is arrestedby the closing valves

In systemic of pulmonary artery hypertension

diastol pressure in respective great artery

velocity of blood surging toward the valve S2 Severe aortic and pulmonary stenosis

the valve commisure are nearly fixed in position

S2


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Changes in splitting in pattern

Widened splitting refers to in the time interval between A2 and P2

the 2 components are audibly separated even

during expiration and become more widely

separated in inspiration

result from delayed closure of the pulmonic valve

(eg. right bundle branch block, pulmonic valve

stenosis)


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Fixed splitting refers to abnormally widened interval between A2

and P2 that persist unchanged through the

respiratory cycle

results fromASD (ASD chronic volume

overload of right-sided circulation

capacitance, resistance pulmonary pressure

delay the backpressure responsible from

closure of pulmonary valve P2 delayed thannormal)


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Paradoxical splitting = Reverse splitting opposite of the normal situation

refers to audible separation of A2 and P2 duringexpiration that disappears on inspiration

the most common cause is Left Bundle BranchBlock (LBBB)

LBBB electrical activity within LV impaired delayed ventricular contraction late closure

aortic valve A2 followed P2 when inspiration, normally P2 occur later and A2

earlier but in LBBB due to A2 delayed P2 andA2 are heard as one sound.


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Extra Systolic Heart Sounds

May occur in early, mid-, or late systole

1. Early Extra Systole Heart Sounds = ejection

clicks

occur shirtly after S1 and coincide with the opening

of the aortic or pulmonic valves

have a sharp, high pitched quality heard best

with the diaphragm of stethoscope, placed over the

aortic and pulmonary areas


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indicate: Aortic or Pulmonic valve stenosis: sound occurs as

the leaflets reach their maximal level of ascent intothe great artery, just prior to blood ejection

Dilatation of the Pulmonary artery or Aorta: sound isassociated with sudden tensing of the aortic orpulmonic root with the onset of blood flow into thevessel aortic ejection click:

Is heard at both base and apex Doesnt vary with respiration

pulmonic Ejection Click: Is heard only at the base

Intensity during inspiration


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2. Mid

or Late Extra Systolic Heart Sounds result of systolic prolapse of the mitral or tricuspid

vein

leaflets bulge abnormally into the atrium during

ventricular contraction.

often accompanied by valvular regurgitation

mitral louder than tricuspid


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Extra Diastolic Heart Sounds

opening snap(OS)

the third heartsound (S3)

the fourth heartsound (S4)

QuadrubpleRythm or

SummationGallop

the pericardial

knock


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Opening Snap

refers to sound that are produced by the mitral ortricuspid valvular stenosis when they open

a sharp, highpitched sound, and timing doesnt

vary significantly with respiration

OS is heard best between apex & left sternalborder, just after the aortic closure sound (A2)

The severity of stenosis can be approximated by

the time interval between A2 and OS :

advanced stenosis interval A2 OS

In mild interval A2 OS


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Third heart sound after S2

result from tensing of the chordae tendinae duringrapid filling and expansion of the ventricle

occurs in early diastole, following the opening of theAV valves during the ventricular rapid filling phase

a dull, low pitched sound best heard with the bell of

the stethoscope S3 normal in children and young adults

implies the presence of a supple ventricle capable ofnormal rapid expansion in early diastole

S3 sign of disease in mid age or older adults

indicating volume overload due to CHF, ortransvalvular flow that accompanies advanced mitral ortricuspid regurgitation

Pathologic S3 Ventricular Gallop

Fourth Heart Sound before


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Fourth Heart Sound beforeS1

is generated by the L or R atrium vigorouslycontracting against the stiffened ventricle

occurs in late diastole and coincides withcontraction of the atria

usually indicates the presence of cardiac disease spesifically ventricular compliance typicallyresult from ventricular hypertrophy or myocardialischemia.

a dull, low pitched sound best heard with thebell

loudest at the apes when patient lying in the L.Lateral decubitus position

S4 atrial gallop


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Quadrubple Rythm or Summation


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Quadrubple Rythm or Summation

Gallop

in patient with S3 and S4 in conjunction with S1and S2 quadrupic beat

if this patient develops tachycardia duration of

diastole S3 and S4 coalesce summation

gallop (heard as as long mid diastolic, low-pitchedsound, often louder than S1 and S2)


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Pericardial Knock

results from the abrupt cessation of ventricularfilling in early diastole

appears early in diastole soon after S2 ; but

slightly later than OS and is louder ; and earlier

than ventricular gallop uncommon, high pitched sound

hall mark of constrictive pericarditis


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Murmurs

the sound generated by turbulent blood flow the mechanisms which produce murmus:

flow across a partial obstruction (eg. Aortic stenosis)

flow through normal structures (eg. Aortic systolic

murmur associated with high output state, anemia) ejection into a dilated chamber (eg. Aortic SM

associated with aneurysmal dilatation of the aorta)

regurgitant flow across an incopetent valve (eg.

Mitral reg) abnormal shunting of blood from 1 vascular

chamber to a lower pressure chamber (eg.

Ventricular septal defect)


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Description of Murmur

1. timing whether murmur occurs during systole,diastole, or continous

2. intensity is typically quantified by a grading systemsystolic murmurs

systo l ic mu rmurs grade 1/6 (or I/VI) : barely audible (eg. medical students may not

hear it) grade 2/6 (or II/VI) : faint but immediately audible grade 3/6 (or III/VI) : easily heard grade 4/6 (or IV/VI) : easily heard and associated with a palpable thrill

grade 5/6 (or V/VI) : very loud; heard with a stethoscope lightly on thechest

grade 6/6 (or VI/VI) :audible without the stethoscope directly on thechest wall

dias to l ic m urmu rs grade 1/4 (or I/IV): barely audible

grade 2/4 (or II/IV): faint but immediately audible

grade 3/4 (or III/IV): easily heard

grade 4/4 (or IV/IV): very loud


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3. pitch frequency of the murmur High are caused by large pressure gradients

between chambers (eg. Aortic stenosis)

Low smaller pressure gradient (eg. Mitral

stenosis)4. shape how the murmur changes in intensity

from its onset to its completion.

CresendoDecresendo (diamond shaped)

Decresendo Uniform (intensity doesnt change shape)


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5. location the murmurs region of maximalintensity

6. radiation murmurs are often heard to radiate

to other areas of the chest from their primary

location7. response to maneuvers maneuvers can alters

the hearts loading conditions and can affect the

intensity of many murmurs.

maneuvers: standing upright, Valsava (forceful

expiration against a closed airway), clenching of

the fist


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Thank you

Cardiac Physical Examination

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