MURMUR

The "murmur" is the sound of blood flowing. It may be passing through a problem heart valve, for
instance. Or it may be that a condition makes yourheart beat faster and forces your heart to handle
more blood quicker than normal.
Most are innocent and don't require any treatment.
But there are exceptions. Murmurs can be linked to a damaged or overworked heart valve. Some
people are born with valve problems. Others get them as a part of aging or from other heart
problems.

Causes
Common conditions can make your heart beat faster and lead to heart murmurs. They can happen
if you're pregnant, or if you have:

 Anemia
 High blood pressure
 Overactive thyroid
 Fever

A murmur could also be a problem with a heart valve. The valves close and open to let blood flow
through the heart's two upper chambers -- called the atria -- and two lower chambers -- the
ventricles. Valve problems include:
Mitral valve prolapse: Normally, your mitral valve closes completely when the lower left chamber
of your heart contracts. It stops blood from flowing back into your upper left chamber. If part of
that valve balloons out so it doesn't close properly, you have mitral valve prolapse. This causes a
clicking sound as your heart beats. It's fairly common and often not serious. But it can lead to the
blood flowing backward through the valve, which your doctor may call regurgitation.
Mitral valve or aortic stenosis: Your mitral and aortic valves are on the left side of your heart. If
they narrow, which doctors call stenosis, your heart has to work harder to pump blood to the rest
of your body. If left untreated, it can wear out your heart and lead to heart failure. You might be
born with this. It can also happen as part of aging, or because of scarring from infections such
asrheumatic fever.
Aortic sclerosis and stenosis: One in three elderly people have a heart murmur because of the
scarring, thickening, or stiffening of their aortic valve. That’s aortic sclerosis. It's usually not
dangerous, since the valve can work for years after the murmur starts. It’s usually seen in people
who have heart disease. But the valve can narrow over time. This is called stenosis. It can lead
to chest pain, shortness of breath, or you may pass out. Sometimes, the valve needs to be replaced.
Mitral or aortic regurgitation: In this case, regurgitation means the blood is going the wrong way
through your mitral or aortic valve and back into your heart. To counteract it, your heart must work
harder to force blood through the damaged valve. Over time, this can weaken or enlarge your heart
and lead to heart failure.
Congenital heart defects: About 25,000 babies are born with heart defects each year. These
problems include holes in heart walls or abnormal valves. Surgery can correct many of them.

Treatment
Many children and adults have harmless heart murmurs, which don't need treatment.
If another condition, like high blood pressure, is causing yours, your doctor will treat the cause.
Some types of heart valve disease may require:

 Medicines to prevent blood clots, controlirregular heartbeat or palpitations, and lowerblood

pressure
 Diuretics to get rid of excess salt and water from your body, making it easier for your heart to
pump
 Surgery to correct heart defects you’re born with
 Surgery to correct certain types of heart valve disease

It's not common, but doctors sometimes ask people to take antibiotics to help prevent heart
infection before dental work or some kinds of surgery.

Diagnosis
Usually, doctors find heart murmurs during aphysical exam. Your doctor will be able to hear it
when listening to your heart with a stethoscope.
Your doctor may order one or more of the following tests to see whether your heart murmur is
innocent or it is caused by acquired valve disease or a defect you were born with:

 Electrocardiogram (EKG), which measures the electrical activity of the heart

 Chest X-rays to see if the heart is enlarged due to heart or valve disease
 Echocardiography, which uses sound waves to map the heart's structure

Prevention?
In most cases, you can't prevent heart murmurs. The exception is that if you treat an underlying
condition, such as high blood pressure, or you avoid heart valve infection, heart murmurs are
stopped before they start.

When to Call Your Doctor

Get medical help if you feel:

 Chest pain
 Breathlessness, fatigue, or fainting for no obvious reason
 Heart palpitations
 Pemeriksaan Radiologi Jantung
Pemeriksaan radiologis jantung dibagi:

 Tanpa kontras ( X foto toraks).

 Dengan kontras (kateterisasi).

Pemeriksaan rutin: X Foto toraks , proyeksi PA dan lateral. Dapat dilengkapi obliq
kanan-kiri, dengan esofagus diisi barium.

Penilaian jantung:

1. Konfigurasi jantung:

 Batas kanan: parasternal.

 Batas kiri: pertengahan klavikula (mid clavicula).
 Batas atas (batas dari arkus aorta): 1 -2 cm di bawah manubrium sterni.
 Batas bawah: sukar ditentukan, karena terdapat diafragma

2. Letak/situs jantung :

 N: jantung di hemitoraks kiri dan fundus jantung di abdomen sisi kiri (situs solitus).
 Dekstrokardia: fundus di kanan,apeks di kanan.
 Dekstroversi: fundus di kiri apeks di kanan.
 Levoversi: fundus di kanan dan apeks di kiri.
 Mesoversi: jantung di tengah-tengah.

3. Ukuran jantung-Cardio Thorak Ratio (CTR):

Memiliki syarat yaitu :

 Posisi PA.
 Inspirasi cukup. Dilihat dari ketinggian diafragma (setinggi costa 9 & 10 posterior yang
berbentuk huruf “A” dan tepi medial jelas dan setinggi costa 5 & 6)
 Bentuk dada normal.
 Tidak ada scoliosis.
 Focus Film Distant: 1,8 – 2 m.
 Keterangan :

 Garis M: garis di tengah-tengah kolumna vertebra torakalis.

 Garis A: jarakantara M dengan batas kanan jantung yang terjauh.
 Garis B: jarakantara M dengan batas kiri jantung yang terjauh.
 Garis C: garis transversal dari dinding toraks kanan ke dinding toraks sisi kiri.

Rumus CTR

Radioanatomi jantung :
Radioanatomi jantung anterior kom

Radioanatomi jantung anterior part

Teknik Pemeriksaan Fisik Jantung

Secara umum, ada empat tahap pemeriksaan fisik yang harus anda jalani untuk memastikan ada
atau tidaknya gangguan pada jantung. Berikut adalah tahapannya:

Inspeksi Jantung
Inspeksi jantung bertujuan untuk menemukan tanda-tanda atau kelainan kondisi jantung melalui
pengamatan pada permukaan dada. Pemeriksaan awal ini biasanya melibatkan empat elemen,
yakni:
o Bentuk prekordium. Pada orang sehat, bentuk kedua belah dada seharusnya simetris.
Perubahan bentuk, seperti cekung dan gembung menunjukkan adanya kelainan.
o Denyut apeks jantung, atau ictus cordis normal hanya berbentuk tonjolan kecil. Jika terjadi
pembesaran atau perluasan, berarti ada indikasi terjadinya kelainan.
o Denyut nadi pada dada. Denyut nadi yang menunjukkan gerakan naik-turun biasanya
menunjukkan adanya pemberasan ventrike; kanan, sedangkan denyutan di bagian atas
menunjukkan adanya kelainan aorta.
o Denyut vena pada dada dan punggung normalnya tidak terlihat. Jika denyutan terlihat,
menunjukkan adanya kelainan.

Palpasi Jantung
Cara pemeriksaan fisik jantung yang kedua ini dilakukan untuk memperkuat hasil temuan inspeksi
fisik. Dalam istilah awam, palpasi berarti meraba; tenaga medis melakukan palpasi menggunakan
telapak tangan atau ujung jari untuk melakukan pemeriksaan pada ictus kordis, getaran, maupun
gerakan trakea. Sebagai contoh, pada keadaan normal, ictus kordis biasanya bisa dipalpasi,
namun pada penderita gangguan jantung, ictus kordis mungkin tidak teraba atau teraba dengan
sangat kuat.

Perkusi
Pemeriksaan ini dilakukan untuk menetapkan batas normal jantung, biasanya dikelompokkan
menjadi batas kiri dan batas kanan jantung. Pada kondisi tertentu, batas jantung meluas ke kanan
atau ke kiri atau mengecil akibat adanya tekanan. Hal ini menunjukkan adanya gangguan.
Sebagai contoh, pada penderita emfisema, batas kanan jantung cenderung mengecil, sedangkan
pada penderita neurisma aorta, daerah jantung meluas ke kanan.

Auskultasi
Pemeriksaan ini dilakukan menggunakan stetoskop duplex. Alat ini berfungsi untuk
mendengarkan bunyi dengan nada rendah pada detak jantung. Bunyi yang terdeteksi
dikelompokkan menjadi 3, yakni Bunyi Jantung I, II, dan bising. Pada penderita gangguan
jantung, seperti penderita obesitas, bunyi jantung mungkin terdengar melemah. Demikian juga
dengan adanya deteksi bising patologis, yang mungkin terjadi akibat pembesaran bilik jantung.

Secara teknis, pemeriksaan ini tentu hanya bisa dilakukan tenaga medis. Untuk itu, sebaiknya
anda berkomunikasi terlebih dahulu dengan dokter (anamnesis), untuk mempermudah tenaga
medis melakukanpemeriksaan fisik jantung dan mengarahkan diagnosis penyakit. Dengan cara ini,
anda akan mendapatkan penanganan yang tepat.

Pemeriksaan Penunjang
Echocardiografi. Diagnosis untuk penyakit jantung koroner dapat dilakukan dengan
pemeriksaan fisik, anamnesis. Pemeriksaan USG jantung dapat dilakukan dengan
ekokardiografi. Sistem ekokardiografi dapat menampilkan, menganalisa dan menangkap hati
secara penuh dalam satu detak jantung.
CT Scan. Perkembangan teknologi telah menciptakan alat baru yaitu Computed
tomography (CT) yang sudah lama berperan penting dalam mendeteksi dini penyakit selama
bertahun-tahun. Semakin berkembangnya teknologi, sehingga dapat menciptakan generasi baru
dengan CT scanner yang dapat melakukan CT angiografi koroner (CTA) dengan mengurangi
dosis radiasi pada pemeriksaan klinis secara rutin.
Pemeriksaan Laboratorium. Selain dengan CT juga dapat menggunakan tes in vitro di
laboratorium, melalui penggunaan biomarker baru yang tarutama dalam perawatan darurat dapat
mempengaruhi dan mendukung keputusan klinis. Pada gagal jantung penggunaan natriuretik
beredar-peptida B (BNP) sangat relevan, karena tingkat biomarker ini adalah indikator yang baik
untuk mengetahui sejauh mana fungsi jantung terganggu. BNP digunakan baik untuk diagnosis
awal dan untuk pemantauan terapi. Pada beberapa pasien, serangan jantung menjadi penyebab
langsung insufisiensi jantung, sehingga deteksi cepat dari infark miokard sangat penting dalam
mencegah bertambah parahnya kerusakan miokard dan kegagalan jantung selanjutnya

Pemeriksaan Apo B dan hs – CRP Kolesterol tinggi bukan satu – satunya penyebab PJK. Kadar
lemak yang tinggi memang merupakan salah satu faktor risiko PJK, namun dalam kenyataannya
ternyata cukup banyak kasus PJK meski kadar lemak normal. Fakta yang terjadi adalah 1 dari 3
kasus serangan jantung terjadi pada orang dengan kadar kolesterol normal. Mengetahui kadar
kolesterol konvensional (Kolesterol Total, Kolesterol LDL – direk, Kolesterol HDL, Trigliserida)
tetap diperlukan, namun ada pemeriksaan lain yang dapat melengkapi penilaian risiko PJK yaitu
Apo B dan hs-CRP. Apo B bermanfaat untuk meningkatkan prediksi risiko PJK, karena semakin
tinggi kadar Apo B, semakin tinggi kemungkinan terjadinya risiko penyumbatan pembuluh darah,
walaupun kadar LDL normal. Hs-CRP bermanfaat untuk meningkatkan prediksi terjadinya
penyakit jantung karena proses aterosklerosis (penyumbatan dan pengerasan pembuluh darah)
yang juga ditandai dengan adanya proses peradangan. Pemeriksaan hs-CRP ini bermanfaat
untuk menentukan risiko kardiovaskular pada individu sehat.

PEREDARAN DARAH JANTUNG JANIN DAN BAYI

PENDAHULUAN

Jantung yang berfungsi sebagai mekanisme pompa mendorong darah melalui seluruh system vaskuler,
sebenarnya terdiri dari dua pompa; jantung kanan yang memompa darah melalui paru-paru, dan jantung
kiri yang memompa darah melalui organ dan jaringan perifer. Masing-masing unit terdiri dari dua ruangan,
atrium dan ventrikel.

System katup mengendalikan aliran darah memlalui pompa ini. Atrium dipisahkan dari ventrikel oleh
katup-katup atrioventrikularis (AV) (katup tricuspid dan katup mitral). Aorta dan arteri pulmonaris
dipisahkan dari ventrikel oleh katup-katup semilunaris (katup aorta dan katup pulmonalis).
Atrium adalah pompa yang lemah. Meskipun membantu pergerakan darah, fungsi utama atrium adalah
sebagai pintu masuk ke ventrikel. Ventrikel memasok tenaga yang diperlukan untuk mendorong darah
melalui sirkualsi pulmonal dan sistemik. Karena jantung kanan dan kiri mempunyai fungsi yang berbeda,
ventrikel kanan dan kiri secara structural tidak identik. Ventrikel kanan (pemasok sirkulais pulmonal)
memompa melawan tahanan yang lebih rendah dan dindingnya lebih tipis daripada ventrikel kiri.
PEREDARAN DARAH PADA JANIN

Peredaran darah janin tidak dapat dipisahkan dari peredaran darah ibu. Sewaktu mudigah tumbuh, pada
permulaan yang mempunyai peranan penting dalam memberikan nutrisi ke embrio (pembentukan dan
peredaran darah janin) adalah yolk sac, yang hanya berfungsi sampai usia kehamilan 10 minggu. Seiring
dengan perkembangan mudigah maka organ-organ tubuh fetus pun mulai terbentuk termasuk di
dalamnya plasenta dan pembuluh darah, sehingga pemberian nutrisi oleh yolk sac pada janin diambil alih
oleh plasenta. Peredaran darah janin berlangsung selama kehidupan intra uteri, di mana plasenta
memegang peranan penting yang menyalurkan darah dari ibu ke janin. Kegagalan fungsi plasenta dapat
menimbulkan berbagai penyulit dalam pertumbuhan dan perkembangan janin. Walaupun organ-organ
janin belum berfungsi, peredaran darah janin berfungsi untuk memenuhi nutrisi untuk pertumbuhan dan
perkembangan janin.

Pada sistem peredaran darah ini akan dibahas tentang : faktor-faktor penentu dalam sistem peredaran
darah janin, komponen/organ yang terlibat, mekanisme dan faktor-faktor penting yang mengubah
peredaran darah janin.

Sirkulasi darah janin dalam rahim tidak sama dengan sirkulasi darah pada bayi dan anak. Dalam rahim,
paru-paru tidak berfungsi sebagai alat pernafasan, pertukaran gas dilakukan oleh plasenta. Sistem
peredaran darah janin ditentukan oleh faktor-faktor sebagai berikut:
1. Foramen Ovale merupakan lubang sementara di antara serambi kiri dan serambi kanan yang
memungkinkan sebagian darah masuk dari vena cava inferior menyeberang ke serambi kiri. Alasan
pengalihan ini adalah darah tidak perlu lagi melewati paru-paru karena telah teroksigenisasi.
2. Duktus Arteriosus Bothall merupakan saluran yang terdapat antara arteri pulmonalis dan aorta.
3. Duktus Venosus Arantii menghubungkan antara vena umbilikal dengan vena cava inferior. Pada titik
ini darah bercampur dengan darah yang telah diambil oksigennya yang kembali dari tubuh bagian bawah.
4. Vena Umbilikal memanjang dari tali pusar menuju ke bagian bawah hati dan membawa darah yang
mengandung oksigen dan sari makanan. Ia memiliki cabang yang bertemu dengan vena porta dan masuk
ke hati.

Komponen/Organ yang Terlibat dalam Pembuluh Darah Janin

Dalam sistem peredaran darah janin tidak hanya melibatkan pembuluh darah saja tetapi juga melibatkan
organ tubuh janin di antaranya sebagai berikut:

1. Plasenta : Tempat terjadinya pertukaran darah bersih dengan yang kotor.

2. Umbilikalis : mengalirkan darah dari plasenta ke janin dan dari janin ke plasenta.
3. Hati : Terdapatnya percabangan antara vena porta dengan duktus venosus arantii.
4. Jantung : Terdapatnya foramen ovale yang langsung menyalurkan darah dari atrium dekstra ke atrium
sinistra.
5. Paru-paru

Terdapatnya duktus arteriosus bothalli.

Mekanisme Peredaran Darah Janin

Peredaran darah janin digambarkan langsung sebagai berikut :

Skema sederhana sirkulasi janin. Daerah gelap menunjukkan saturasi oksigen darah, dan panah
menunjukkan perjalanan sirkulasi janin. Organ tidak digambarkan dengan skala. Tiga pirau yang
memungkinkan sebagian besar darah memintas hati dan paru-paru: (1) duktus venosus, (2) foramen
ovale, dan (3) duktus arteriosus.
Mekanisme Peredaran Darah Janin (Sirkulasi Darah Fetus)
Keterangan gambar :
Mula-mula darah yang kaya akan oksigen dan nutrisi yang berasal dari plasenta masuk ke janin melalui
vena umbilikus yang bercabang dua setelah memasuki dinding perut yaitu :
a. Cabang yang kecil bersatu dengan vena porta, darahnya beredar dalam hati dan kemudian diangkut
melalui vena hepatika ke vena cava inferior.
b. Cabang satunya lagi duktus venosus arantii yang langsung masuk ke dalam vena cava inferior. Darah
dari vena cava inferior masuk ke atrium kanan dan sebagian besar darah dari atrium kanan akan dialirkan
ke atrium kiri melalui foramen ovale. Sebagian kecil darah dari atrium kanan masuk ke ventrikel kanan
bersama-sama dengan darah yang berasal dari vena cava superior. Darah dari ventrikel kanan ini
dipompakan ke paru-paru melalui arteri pulmonalis, karena adanya tahanan dari paru-paru yang belum
mengembang maka darah yang terdapat pada arteri pulmonalis sebagian akan dialirkan ke aorta melalui
duktus arteriosus bothalli dan sebagian kecil akan menuju paru-paru dan selanjutnya ke atrium sinistra
melaui vena pulmonalis. Sementara itu darah yang terdapat pada atrium kiri kemudian dialirkan ke
ventrikel kiri dan diteruskan ke seluruh tubuh melaui aorta guna memberikan oksigen dan nutrisi bagi
tubuh bawah. Cabang aorta bagian bawah ini menjadi 2 (dua) arteri hipograstika interna yang mempunyai
cabang arteri umbilikalis.
Darah yang miskin nutrisi dan banyak karbondioksida serta sisa metabolisme akan dikembalikan ke
plasenta melalui arteri umbilikalis ke plasenta melalui arteri umbilikalis untuk mengadakan pertukaran
gas selanjutnya. Foramen ovale dan duktus arteriosus berfungsi sebagai saluran/jalan pintas yang
memungkinkan sebagian besar dari cardiac output yang sudah terkombinasi kembali ke placenta tanpa
melalui paru-paru.

C. PEREDARAN DARAH PADA BAYI

Semasa kehidupan janin, aliran darah pulmonal adalah sekitar 10% sampai 15% dari campuran keluaran
ventrikel; paru-paru dua pertiganya terisi cairan; dan tahanan pembuluh darah pulmonal tinggi akibat
rendahnya kandungan oksigen darah rendah (PO2).
Ketika bayi lahir, paru-parunya segera mengembang. Alveolus berisi udara dan tahanan pembuluh darah
pulmonal turun mendadak dan dramatis (meskipun tidak mencapai tingkat dewasa pada usia enam
sampai delapan minggu). Pada saat yang sama, tekanan aorta meningkat karena aliran darah ke plasenta
mendadak berhenti. Tekanan pulmonal menurun, tekanan aorta meningkat, dan darah yang telah
mengalir ke depan dari arteri pulmonalis melalui duktus arteriosus ke aorta, mendadak mulai mengalir
balik ke belakang, dari aorta melalui duktus ke arteri pulmonalis. Perubahan ini terjadi dalam beberapa
jam.
Sebelum lahir, duktus arteriosus tetap terbuka kemungkinan karena pengaruh prostaglandin, suatu
hormone yang ditemukan dalam dindingnya, meskipun mekanisme yang pasti belum diketahui. Duktus
arteriosus menutup, sepuluh sampai 15 jam setelah kelahiran bayi cukup bulan yang normal, dan darah
yang mengalir melaluinya berhenti. Pencetus penutupan mungkin terjadinya peningkatan tekanan
oksigen arterial pascalahir. Walaupun demikian, belum jelas apakah oksigen mempengaruhi sel otot polos
duktus secara langsung, atau apakah terlibat zat tambahan. Kadang-kadang duktus arteriosus
membutuhkan waktu beberapa minggu untuk menutup sempurna, dan satu dari setiap 5.500 bayi,
duktusnya tidak pernah menutup.
Perubahan sirkulasi lainnya yang terjadi saat kelahiran adalah pada septum atrium, dinding yang
memisahkan atrium kiri dan kanan. Sebelum kelahiran, aliran darah yang mengalir ke dalam jantung dari
vena kava inferior dibagi antara atrium kanan dan kiri oleh bagian dari septum atrium, tepi atas septum
primum. Terdapat lebih banyak oksigen (lebih sedikit campuran darah vena) pada atrium kiri karena aliran
darah beroksigen tinggi dari vena kava inferior hanya di encerkan sedikit oleh darah deoksigenasi dari
paru-paru janin. Setelah kelahiran, tekanan dalam atrium kiri meningkat karena peningkatan aliran darah
di atrium kiri akibat peningkatan aliran vena pulmonalis. Tekanan atrium kanan menurun karena
penurunan tahanan pembuluh darah pulmonal. Septum atrium, yang berkonstruksi seperti katup satu
arah menutup, mencegah aliran balik darah dari kiri ke kanan.
Semasa kehidupan janin, darah yang mengalir melalui foramen ovale dari kanan ke kiri; pascalahir, aliran
biasanya kiri ke kanan. Walaupun demikian, dalam situasi dimana tekanan atrium kanan melampaui
tekanan atrium kiri, seperti pada stenosis pulmonal atau atresia pulmonal, atresia tricuspid, atau
hipertensi pulmonal persisten, darah terus mengalir dari kanan ke kiri pada kehidupan pascalahir melalui
defek septum atrium.

Mekanisme Peredaran Darah Bayi

Peredaran darah bayi digambarkan langsung sebagai berikut :

Skema sederhana sirkulasi bayi. Terlihat sisa pembuluh darah dan struktur janin pada orang dewasa yang
tidak berfungsi sejak lahir, dan panah menunjukkan perjalanan sirkulasi neonates. Organ tidak digambar
dengan skala. Setelah lahir, ketiga pirau yang memintaskan darah sewaktu kehidupan janin berhenti
berfungsi, dan sirkulasi pulmonal dan sistemik menjadi terpisah.
Faktor-Faktor yang Mengubah Peredaran Darah Janin
Setelah kelahiran terjadi perubahan peredaran darah janin, faktor penting yang mengubah peredaran
darah janin menuju peredaran darah dewasa ditentukan oleh:
1. Berkembangnya paru-paru janin
Berkembangnya paru-paru janin dapat menyebabkan tekanan negatif dalam paru sehingga dapat
menampung darah, untuk melakukan pertukaran CO2 dan O2 dari udara sehingga terjadi oblitersi pada
 duktus arteriosus bothalli. Tekanan dalam atrium kiri makin meningkat, sehingga dapat menutup foramen
ovale. Tekanan yang tinggi pada atrium kiri disebabkan darah yang mengalir ke atrium kanan kini langsung
menuju paru-paru dan selanjutnya dialirkan ke atrium kiri melalui vena pulmonalis. Dua faktor ini
menyebabkan tekanan di atrium kiri meningkat.
2. Terputusnya hubungan peredaran darah antara ibu dan janin
Terputusnya hubungan peredaran darah antara ibu dan janin terjadi karena dipotongnya tali pusat
sehingga terjadi peredaran darah pulmonal yang mengakibatkan terjadi pernafasan pulmona. Dengan
demikian duktus arteriosus bothalli tidak berfungsi dan akan mengalami perubahan dan menjadi
ligamentum arteriosum begitu juga dengan yang lain. Vena umbilikal menjadi ligamentum teres, duktus
venosus arantii menjadi ligamentum venosum serta foramen ovale menjadi hypogastrik arteries kecuali
beberapa cm pertama yang tetap terbuka sebagai arteri vesical superior. Pemotongan tali pusat sebaiknya
dilakukan setelah bayi menangis dan tali pusat berhenti berdenyut karena dapat menambah darah dari
plasenta sekitar 50 ml s/d 75 ml yang sangat berarti bagi pertumbuhan janin.
3. Terbentuknya Adult Haemoglobin (Tipe A)
Terbentuknya Adult Haemoglobin (Tipe A) sehingga setelah lahir dapat menangkap oksigen dan
melepaskan CO2 melaului pernafasan sehingga terjadi pertukaran O2 dan CO2 di paru-paru.

Sirkulasi Darah Janin

Perubahan mendadak dari kehidupan intrauterine ke ekstrauterin memerlukan penyesuaian sirkulasi
neonatus berupa :

 pengalihan aliran darah dari paru,

 penutupan ductus arteriosus Bottali dan foramen ovale serta
 obliterasi ductus venosus Arantii dan vasa umbilikalis.
Sirkulasi bayi terdiri dari 3 fase :

1. Fase intrauterin dimana janin sangat tergantung pada plasenta

2. Fase transisi yang dimulai segera setelah lahir dan tangisan pertama
3. Fase dewasa yang umumnya berlangsung secara lengkap pada bulan pertama kehidupan
1. Fase intrauterin

Vena umbilikalis membawa darah yang teroksigenasi dari plasenta menuju janin (gambar 2 dan 3 )

Lebih dari 50% cardiac out-put berjalan menuju plasenta melewati arteri umbilikalis. Cardiac out-put terus
meningkat sampai aterm dengan nilai 200 ml/menit. Frekuensi detak jantung untuk mempertahankan
cardiac output tersebut 110 – 150 kali per menit.

Tekanan darah fetus terus meningkat sampai aterm, pada kehamilan 35 minggu tekanan sistolik 75 mmHg
dan tekanan diastolik 55 mmHg

Sel darah merah, kadar hemoglobin dan “packed cell volume” terus meningkat selama kehamilan.
Sebagian besar eritrosit mengandung HbF
 Pada kehamilan 15 minggu semua sel darah merah mengandung HbF. Ada kehamilan 36 minggu, terdapat
70% HbF dan 30% Hb A.

HbF memiliki kemampuan mengikat oksogen lebih besar dibanding HbA. HbF lebih resisten terhadap
hemolisis namun lebih rentan terhadap trauma.

2. Fase transisi

Saat persalinan, terjadi dua kejadian yang merubah hemodinamika janin

1. Ligasi talipusat yang menyebabkan kenaikan tekanan arterial

2. Kenaikan kadar CO2 dan penurunan PO2 yang menyebabkan awal pernafasan janin
Setelah beberapa tarikan nafas, tekanan intrathoracal neonatus masih rendah (-40 sampai – 50 mmHg) ;
setelah jalan nafas mengembang, tekanan meningkat kearah nilai dewasa yaitu -7 sampai -8 mmHg.

Tahanan vaskular dalam paru yang semula tinggi terus menurun sampai 75 – 80%. Tekanan dalam arteri
pulmonalis menurun sampai 50% saat tekanan atrium kiri meningkat dua kali lipat.

Sirkulasi neonatus menjadi sempurna setelah penutupan ductus arteriousus dan foramen ovale
berlangsung, namun proses penyesuaian terus berlangsung sampai 1 – 2 bulan kemudian.

3. Fase Ekstrauterin

Ductus arteriousus umumnya mengalami obliterasi pada awal periode post natal sebagai reflek adanya
kenaikan oksigen dan prostaglandin.

Bila ductus tetap terbuka, akan terdengar bising crescendo yang berkurang saat diastolik (“machinery
murmur”) yang terdengar diatas celah intercosta ke II kiri.

Obliterase foramen ovale biasanya berlangsung dalam 6 – 8 minggu. Foramen ovale tetap ada pada
beberapa individu tanpa menimbulkan gejala. Obliterasi ductus venosus dari hepar ke vena cava
menyisakan ligamentum venosum. Sisa penutupan vena umbilikalis menjadi ligamentum teres hepatis.

Hemodinamika orang dewasa normal berbeda dengan janin dalam hal :

1. Darah vena dan arteri tidak bercampur dalam atrium

2. Vena cava hanya membawa darah yang terdeoksigenasi menuju atrium kanan, dan selanjutnya menuju
ventrikel kanan dan kemudian memompakan darah kedalam arteri pulmonalis dan kapiler paru
3. Aorta hanya membawa darah yang teroksigenasi dari jantung kiri melalui vena pulmonalis untuk
selanjutnya di distribusikan keseluruh tubuh janin.

THE FETAL CIRCULATION SYSTEM

The two cardiac shunts:

 Connection between the right and left atria via the foramen ovale 
 Connection between the truncus pulmonalis and the aorta via the
ductus arteriosus
From the parallel blood flow pathways through the heart together with the two shunts the
following circulation system results: The blood from the placenta that has been enriched with
oxygen and nutrients gets via the umbilical vein to the liver, part flows through it and part
bypasses it via the ductus venosus and gets via the v. cava inferior into the right atrium.

There are indications that a functional sphincter regulates the flow of blood through
the ductus venosus. The umbilical vein transports nutrient-rich blood from the placenta and a
large part of it is channeled through the bed of capillaries in the liver. Due to periodic
contractions of the uterus, the pressure in the umbilical veins increases and more nutrient-rich
blood gets directly via the ductus venosus into the inferior vena cava. Relaxation of the uterine
musculature leads to a decrease in umbilical vein pressure and blood deriving from the fetal
circulation and from the hepatic vein flows into the inferior vena cava and thereby into the right
atrium.

The largest part of the blood from the right atrium flows via the foramen ovale into the left atrium
and via the mitral valve into the left ventricle.
From there it empties into the aorta, which winds around the truncus pulmonalis (ascending
aorta), glides over the bifurcation in the right and left pulmonary artery (aortic arch), and – heading
towards the back - goes over into the descending part of the aorta. In contrast, CO2-rich, nutrient-
poor blood flows from the superior vena cava into the right atrium, is partially mixed with the O 2-
rich blood from the placenta and, via the tricuspidal valve, gets into the right ventricle. Via
the pulmonary trunc and thepulmonary arteries a small portion of the blood passes through
the pulmonary circulation and, via the pulmonary veins, reaches the left atrium and then the
large circulation system. Due to the high pressure in the lungs, though, a significantly larger part
flows through the ductus arteriosus and goes into the aorta descendens and thus directly into
the large (systemic) circulation system.
Due to the higher pressure of the blood in the inferior vena cava, more blood flows from it directly
into the left atrium via the foramen ovale.
The foramen ovale opens like a valve and can direct the blood stream that comes from below
directly into the left atrium. Taken together, the diameters of the inferior and superior vena cava
are larger than that of the foramen ovale and therefore a small portion of the blood seeps into the
right ventricle via the tricuspid valve. The heart is filled only with a mixed blood (O2 saturation).

CHANGES AT BIRTH
With birth, a change from parallel flow through the heart to a serial one gradually takes place. The
following changes must occur:

1. The gas exchange takes place in the baby's lungs.

2. By cutting the umbilical cord, the placental circulation system is switched off.
3. The fetal heart shunts become closed.

With the activation of breathing the lungs becomes distended, the capillary network dilated and
their resistance is reduced drastically so that a rich flow of blood can take place. As a
consequence, the pressure in the right atrium sinks in comparison with that of the left one.
This pressure turnaround in the atria causes the septum primum to be pressed against the
septum secundum and the foramen secundum becomes functionally closed. Towards the end
of the first year, it has also grown together in 99% of the babies --> The shunt between the left
and right atrium is closed.

On the other hand, with the cutting of the umbilical cord following birth, the placental low
resistance area also disappears and the peripheral resistance increases in the systemic
circulation. The pressure in the aorta is now higher than that in the truncus pulmonalis and the
right-left shunt via the ductus arteriosus that is present before birth is turned around into being
a left-right shunt. The pO2 pressure in the aorta increases since the blood is now oxygenated
directly in the baby's lungs. This increase in pO2triggers a contraction of the smooth musculature
in the wall of the ductus arteriosus and thereby to a functional seal.

After a few weeks or months this shunt via the ductus arteriosus is definitively obliterated and
the remnant is known as the ligamentum arteriosus.

The severing of the baby's umbilical cord leads to the obliteration of the umbilical vessels,
primarily through active constriction of their muscular layer. Only the proximal part of the umbilical
arteries stays open as the superior vesical artery. The distal part forms the medial umbilical
ligament on both sides in the anterior abdominal wall. The umbilical vein transforms itself into
the ligamentum teres hepatis.

HEART SOUNDS
Cardiovascular diseases continue to be the leading cause of morbidity and mortality worldwide.
One of the first steps in evaluating the cardiovascular system after detailed history taking is
physical examination. Auscultation of the heart forms the core of cardiac physical examination.
Despite significant interobserver variability and need for habituation and training, cardiac
auscultation provides important initial clues in patient evaluation and serves as a guide for further
diagnostic testing.
Some of the common mechanisms by which heart sounds are generated include (1) opening or
closure of the heart valves, (2) flow of blood through the valve orifice, (3) flow of blood into the
ventricular chambers, and (4) rubbing of cardiac surfaces.
The main anatomic areas to focus on while initially evaluating heart sounds include the cardiac
apex, the aortic area (second intercostal space [ICS] just to the right of the sternum or the third
ICS just to the left of sternum), the pulmonary area (second ICS just to the left of sternum) and
the tricuspid area (fourth and fifth ICS just to the left of sternum).[1] In addition, auscultation of the
left axilla, base of the heart, carotid arteries, and interscapular area should be performed to assess
for radiation of heart sounds and murmurs.
The patient should be examined in the supine position, in the left lateral decubitus position, and
while sitting and leaning forward. Each area should be systematically auscultated for S1, S2,
physiologic splitting, respiratory variations, and any accessory sounds during systole and
diastole.[2] Whenever possible, auscultation should be accompanied by having the patient perform
dynamic maneuvers such as standing, Valsalva, squatting, and hand grip, although these
maneuvers are falling out of favor with the use of echocardiography.
FIRST HEART SOUND
The first heart sound (S1) is produced by vibrations generated by closure of the mitral (M1) and
tricuspid valves (T1).[3] It corresponds to the end of diastole and beginning of ventricular systole
and precedes the upstroke of carotid pulsation. Refer to the audio example below.
The normal heart sound demonstrating S1 followed by an S2, best audible at the apex. Audio
courtesy of 3M™ Littmann® Stethoscopes. (MP3)
M1 is best heard over the apex of the heart, and T1 is best heard over the fourth ICS at the left
sternal border.
Typically, S1 is a high-pitched sound best heard with the diaphragm of the stethoscope. The
intensity of S1 depends on the integrity and pliability of valvular cusps, the length of the PR interval
(which governs the velocity of valve closure), the strength of ventricular contraction, the presence
or absence of valvular stenosis or regurgitation, the position of the valve leaflets at end-diastole,
and the amount of tissue between the heart and the stethoscope. The role of these factors is
discussed as below.[1, 4, 5]
The pliability of the valve cusps governs the ease of valvular apposition and closure. With an
increased degree of calcification and fibrosis, pliability is lost, leading to diminished valvular
mobility and diminished S1. This can happen in advanced rheumatic mitral stenosis (MS) and
postradiation MS.
S1 is influenced by ventricular contractility. Positive inotropic forces lead to a rapid rise in
ventricular pressure and a loud S1. A sharp rise in ventricular pressure causes more rapid
increase in ventricular pressure relative to atrial pressure and a faster closure of atrioventricular
(AV) valves, leading to louder S1. Similarly, negative inotropic forces lead to a diminished rate of
rise in ventricular pressure and a diminished S1.
The PR interval governs the time that atria have to empty their contents into the ventricle. With a
short PR interval, the atria have less time to empty into the ventricle, which leads to more forceful
atrial contraction and maximal separation of the AV valves, leading to louder S1 upon valvular
closure. In addition, the tachycardia associated with a short PR interval leads to a faster rise of
ventricular systolic pressure relative to atrial pressure, with forceful closure of the AV valves and
a loud S1. Similarly if the PR interval is prolonged, the atria have time to slowly empty into the
ventricles, and the AV valves are less separated by the end of atrial contraction, leading to less
forceful closure of AV valves and a lower intensity S1.
The valvular position at the end of ventricular diastole also determines the intensity of S1. The
farther apart the leaflets are at the beginning of systole, the more rapid is their closure and the
louder is S1. Similarly, the closer the leaflets are to each other at the beginning of the systole, the
shorter the distance of travel required for valvular apposition and the softer the S1. The leaflets
are far apart with increased transvalvular gradient (ie, MS or tricuspid stenosis [TS]), increased
transvalvular flow (ie, with left-to-right intracardiac shunts at the level of the ductus or ventricle),
tachycardia, and preexcitation syndromes.
With AV valvular regurgitation, the leaflets are not able to appose properly, leading to a muffled
S1. In acute aortic regurgitation (AR), left ventricular (LV) end-diastolic pressure rapidly rises; thus,
there is faster equilibration of ventricular and atrial pressures, leading to early closure of mitral
valve and a muffled S1.
 The S1 is muffled when there is an increased amount of tissue between the heart and the
stethoscope, as occurs with pleural effusion, pericardial effusion, emphysema, pneumothorax,
and obesity. Similarly, in thin-walled individuals, the heart is closer to the chest wall, and the
sounds are better transmitted to the stethoscope, leading to a louder S1.
Conditions associated with a loud S1 include the following:
 Increased transvalvular gradient (MS, TS, atrial myxoma)
 Increased force of ventricular contraction (tachycardia, hyperdynamic states [ie, anemia, fever,
thyrotoxicosis, exercise, inotropic agents])
 Shortened PR interval - Tachycardia, preexcitation syndromes (ie, Wolff-Parkinson-White
[WPW] syndrome)
 Mitral valve prolapse (MVP), thin individuals
S1 can have a variable intensity in conditions that produce variable PR interval or variable
ventricular contractility. This can happen in Mobitz type I heart block, digitalis toxicity, atrial
fibrillation, and ventricular tachycardia with AV dissociation.
Conditions associated with diminished intensity of S1 include the following:
 Inappropriate apposition of the AV valves (ie, mitral regurgitation [MR], tricuspid regurgitation
[TR], dilated cardiomyopathy)
 Prolonged PR interval (ie, bradycardia, heart block, digitalis toxicity)
 Decreased force of ventricular contraction (ie, cardiomyopathy, myocarditis, myxedema,
myocardial infarction [MI])
 Increased calcification of the AV valve (ie, calcific MS, postirradiation)
 Increased distance from the heart (ie, obesity, emphysema, pleural effusion, pericardial
effusion)
Split S1
Normally, the mitral valve closes just prior to the tricuspid valve. Thus, M1 is audible before T1 (a
difference that is often not detectable).
Splitting of S1 is more prominent when the time difference between the closure of the mitral and
the tricuspid valves is increased. This can happen with early closure of the mitral valve or a
delayed closure of the tricuspid valve relative to the mitral valve.
Some of the conditions associated with a split S1 include the following:
 Premature ventricular contractions (PVCs) of LV origin
 Right bundle branch block
 LV pacing
 Ebstein anomaly
 Atrial septal defect (ASD)
Additionally, in severe TS, the tricuspid valve closes after the mitral valve; this difference can be
perceived on auscultation.
Reverse splitting of S1 occurs when M1 follows the closure of T1. This happens when the closure
of mitral valve is delayed as can happen with left bundle branch block, right ventricular (RV)
pacing, severe MS, and left atrial myxoma.
SECOND HEART SOUND
The second heart sound (S2) is produced by the closure of the aortic (A2) and the pulmonary
valves (P2) at the end of systole.[6] Refer to the audio example below.
The normal heart sound demonstrating S1 followed by an S2, best audible at the apex. Audio
courtesy of 3M™ Littmann® Stethoscopes. (MP3)
A2 is best heard at the aortic area (second right intercostal space); P2 is best heard at the
pulmonary area. S2 is a high-pitched sound heard best with the diaphragm of the stethoscope.
The intensity depends on valvular factors, the transvalvular gradient, mechanical factors, and size
of the great vessels.
Intensity of aortic component
The intensity of A2 is increased with systemic hypertension, in coarctation of the aorta, in aortic
aneurysm, in thin individuals, and when the aorta is closer to the anterior chest wall as may occur
with tetralogy of Fallot and transposition of the great arteries (TGA).
Theintensity of A2 is decreased with decreased aortic diastolic pressure (as in AR), with improper
valvular apposition (as can occur with AR or aortic dissection), calcific immobile valves (as may
occur with calcific aortic stenosis [AS]), and decreased systemic arterial pressure.
Intensity of pulmonic component
The intensity of P2 is increased with pulmonary arterial hypertension[7] from any etiology. A loud
P2 is also audible with ASD,[8] although the exact mechanism in this condition remains unclear.
Split S2
Normally, the aortic valve closes slightly before the pulmonary valve. This difference is more
pronounced with inspiration due to increased RV stroke volume.
S2 splitting results from the aortic valve closing slightly before the pulmonary valve, and this is
more prominent with inspiration. The pulmonary and the aortic valves remain open briefly after
the end of systole and after the LV and RV pressures have been lowered compared to aortic
pressures. This interval between the actual valve closure and pressure crossover between
ventricles and great vessels has been called the hangout time.[1] , which is inversely proportional
to the resistance to blood flow in the great vessels. The pulmonary vascular resistance is less
than the systemic vascular resistance. Thus, the hangout time is longer for the pulmonic valve
than for the aortic valve. This accounts for delayed closure of pulmonary valve relative to the
aortic valve.
With inspiration, pulmonary arterial resistance further declines, leading to further delay in
pulmonary valve closure and a more pronounced split.[9] Another factor contributing to the delayed
closure of pulmonary valve with inspiration is prolonged RV emptying time due to increased stroke
volume as a result of increased preload with inspiration.
Wide S2 splitting
Normally, with expiration, S2 is single, as the aortic and the pulmonary valve closures occur almost
simultaneously. If, at expiration, the two different components of S2 can still be appreciated
separately, then S2 is said to be widely split.
The wide split can result from delayed closure of the pulmonary valve or early closure of the aortic
valve during expiration.
Delayed closure of pulmonary valve can result from conduction or hemodynamic abnormalities.
Delayed electrical activation of the RV accounts for a delayed onset of systole, with delayed
completion of RV emptying and thus delayed closure of the pulmonary valve. This can happen
with right bundle branch block, LV pacing, PVCs arising from the left ventricle, and WPW with
preexcitation of the left ventricle. Hemodynamic reasons for delayed closure of the pulmonary
valve include RV outflow obstruction (pulmonary valvular, supravalvular, or subvalvular stenosis),
pulmonary hypertension, and pulmonary artery branch stenosis.
Early closure of the aortic valve occurs with early emptying of the left ventricle, as can happen
with MR or with ventricular septal defect (VSD) with left–to-right shunting.
With widening of the S2 split, the respiratory variability is preserved (ie, with inspiration, the split
becomes wider compared to expiration).
Wide fixed splitting
The split S2 is said to be widely fixed when the respiratory variability in the relation of A2 -P2 is lost
and the time interval between A2 and P2 remains relatively constant, with P2 following A2. This
occurs most commonly ASD with left-to-right shunting but can also occur with right ventricular
failure.
The exact mechanism of the fixed-split S2 in ASD is unknown, but it is postulated that the RV
systolic time remains relatively constant (ie, there is a loss of respiratory variability in RV stroke
volume). In the presence of ASD with left-to-right shunt, the RV stroke volume is composed of
contributions from the superior vena cava (SVC) and the left atrium. During inspiration, the
contribution from the SVC is increased owing to increased blood flow from the body to the heart.
During expiration, there is a greater flow across the atrial shunt. Thus, the net RV stroke volume
remains constant throughout the respiratory cycle.
Conditions associated with RV failure may also cause fixed splitting of S2 by compromising the
ability of RV to alter its stroke volume with respiration. This can occur with primary RV failure,
pulmonary hypertension, and RV outflow tract obstruction.
Reverse splitting
When the A2 is audible after P2 during expiration, S2 is said to be paradoxically split. This can
happen when the RV contraction is completed before LV contraction. This can result from
conduction or hemodynamic reasons.
Reverse splitting due to conductive disturbance occurs in conditions that cause delayed activation
(and thus delayed emptying) of the left ventricle, such as left bundle branch block, RV pacing,
PVCs of RV origin, and preexcitation of the RV in WPW syndrome.
Reverse splitting due to hemodynamic reasons may occur with delayed emptying of the LV, as
can occur with LV outflow tract obstruction caused by AS.

While interpreting the heart sounds, it is essential to understand from which part of the cardiac
cycle they are being generated. This can be done by palpating the carotid artery simultaneously
while auscultating the heart. The carotid upstroke corresponds to ventricular systole.
 THIRD HEART SOUND
The third heart sound (S3) is a low-pitched, early diastolic sound audible during the rapid entry of
blood from the atrium to the ventricle. When arising from the LV, it is best audible at the apex with
the patient in left lateral decubitus position with breath held at end expiration. When it is of RV
origin, S3 is best audible at the left lower sternal border or the xiphoid with the patient in supine
position. These are best heard with the bell of the stethoscope. Refer to the audio example below.
The low-pitched third heart sound as audible at the apex. Audio Courtesy of 3M™ Littmann®
Stethoscopes. (MP3)
The exact mechanism of genesis of S3 is debatable. Some of the proposed mechanisms are listed
below.[10, 11, 12]
S3 occurs when rapidly rushing blood flow from the atria is suddenly decelerated by the ventricle
when it reaches its elastic limit. In a normal ventricle, this can happen with excessive volume of
incoming blood, as can happen in hyperdynamic states or volume-loaded conditions. Similarly, in
a ventricle that is already stretched and overfilled owing to systolic dysfunction, even a relatively
normal (or less than normal) amount of blood entry can stretch the ventricle enough for it to reach
its elastic limit. With decreased compliance of the ventricle, as can happen with hypertrophy and
diastolic dysfunction, a normal amount of blood entry during diastole can challenge ventricular
elasticity and generate the S3.
Movement of ventricle closer to the chest wall (the so-called “impact theory”): When the ventricle
is dilated, it moves closer to the chest wall. This close proximity of the ventricle to the chest wall
leads to a more forceful impact with entry of blood during diastole.
S3 can be physiologically present in patients younger than 40 years. These patients often have a
thin chest wall to permit the easy transmission of S3. In the presence of heart failure, S3 is a bad
prognostic sign.[13] Conditions associated with pathological S3 include the following:
 Systolic and/or diastolic ventricular dysfunction
 Ischemic heart disease
 Hyperkinetic states - Anemia, fever, pregnancy, thyrotoxicosis, AV fistula
 MR or TR
 Chronic AR with systolic dysfunction
 Systemic and pulmonary hypertension
 Acute aortic regurgitation
 Volume overload - Renal failure

FOURTH HEART SOUND

The fourth heart sound (S4) is a late diastolic sound that corresponds to late ventricular filling
through active atrial contraction. It is a low-intensity sound heard best with the bell of the
stethoscope. When of LV origin, S4 is best heard at the apex with the patient in the left lateral
decubitus position at end expiration. When of RV origin, it is heard best at the left lower sternal
border. Maneuvers that increase the preload increase the intensity of S4 by increasing the
separation of S4 from S1. Left-sided S4 is also augmented by increased afterload as can happen
with hand grip. Refer to the audio example below.
The low-pitched diastolic heart sound audible just before S1 in the cardiac cycle. Audio courtesy
of 3M™ Littmann® Stethoscopes. (MP3)
 The exact mechanism of S4 generation is debatable. The ventricular theory proposes that S4 is
generated by sudden deceleration of the jet of blood as it enters a ventricle with decreased
compliance. The impact theory proposes the movement and impact of the ventricle on the chest
wall as the jet of blood from atrial systole strikes the ventricle. In either case, active atrial
contraction is necessary for the generation of S4. Thus, S4 is not audible with atrial fibrillation or
flutter.
Some of the conditions associated with S4 include the following:
 Ventricular hypertrophy - LV hypertrophy (systemic hypertension, hypertrophic cardiomyopathy,
AS) [14] ; RV hypertrophy (pulmonary hypertension, pulmonary stenosis [PS])
 Ischemic heart disease - Acute MI, [15] angina
 Ventricular aneurysm
 Hyperkinetic states that cause forceful atrial contraction
Both S3 and S4 need to be differentiated from splitting of the normal heart sounds. With splitting,
the heart sounds are high pitched and best audible with the diaphragm, whereas the S3 or S4 are
low-pitched sounds best audible with the bell of the stethoscope.

OPENING SNAP
The opening snap (OS) is a high-pitched diastolic sound produced by rapid opening of the mitral
valve in MS or tricuspid valve in TS.[16] When mitral in origin, it is best heard at the apex following
the aortic sound A2, with the patient in left lateral decubitus position.
The time difference between the A2 and OS has a diagnostic implication. The closer the OS is to
A2, the more severe the stenosis. The OS signifies the time moment when the left atrial pressure
exceeds the LV diastolic pressure and marks the beginning of blood entry into the LV from the
LA. The more severe the stenosis, the greater the LA pressure and the lesser the LA-LV early
diastolic pressure gradient, leading to an early opening of the respective valve. In general, the
relation between A2 and the OS depends on LV pressure at A2 closure, LA pressure at A2 closure,
and the rate of LV pressure decline.[17]
The A2 -OS interval can be increased despite severe MS in patients who have systemic
hypertension with an early closure of AV.
TS usually occurs in association with MS, and, as such, the findings are generally obscured by
the findings of MS.

Ejection Systolic Sounds

The ejection systolic sounds are heard during the early part of ventricular systole. These sounds
are generally high pitched and best audible with the diaphragm of the stethoscope. They can be
valvular or vascular in origin.
Valvular ejection sounds
These are the systolic sounds that are audible in patients with defects in aortic or pulmonary
valves. They are present in early systole after the S1. The aortic ejection sound is best audible at
the apex or the aortic area. The pulmonary valve ejection sound is best audible at the pulmonary
area.
The aortic valvular ejection sound is associated with bicuspid aortic valves and aortic
regurgitation. Pliable valves generate a higher-intensity ejection click. The intensity of the ejection
click decreases with increased valvular calcification. Thus, the aortic ejection click may be absent
in severe calcific AS.[18] The ejection click is also absent in supravalvular or subvalvular AS. The
presence of an aortic ejection sound, in the absence of other signs of AS, strongly suggests the
presence of a bicuspid aortic valve.[19]
The pulmonary valvular ejection sound is predominantly associated with pulmonary valvular
stenosis.[20] Unlike most right-sided sounds, the ejection click of PS is decreased in intensity with
inspiration. One of the proposed mechanisms is a rapid opening of the valve from the closed
position with expiration, giving rise to the high-intensity sound. With inspiration, the rapid jet from
the right atrium can partially open the pulmonary valve during diastole; thus, the opening of
pulmonary valve with the onset of RV systole is more gradual, leading to decreased intensity of
the sound.
Vascular ejection sounds
These sounds are produced at the aorta or pulmonary artery.
The aortic vascular ejection sounds are associated with aortic sclerosis with tortuous aortic root,
systemic hypertension, ascending aortic aneurysm, and aortic root dilatation. This sound is
usually audible at the aortic area and is not well transmitted to the apex.
The pulmonary vascular ejection sound is associated with pulmonary hypertension and
pulmonary arterial dilatation. It is best audible at the left second and third intercostal area.
Nonejection systolic click
This is associated with mitral or tricuspid valve prolapse. Of the two entities, MVP is more
common. Refer to the audio example below.
The mid-systolic click from mitral valve prolapse. Audio courtesy of 3M™ Littmann®
Stethoscopes. (MP3)
The nonejection systolic click is a high-pitched systolic sound that follows S1 and is heard best at
the apex (MVP) or the tricuspid area (tricuspid valve prolapse) with the diaphragm of the
stethoscope. The interval between S1 and the prolapse click may vary depending on the volume
status of the respective ventricles, as the prolapse occurs at a specific ventricular volume.[21] .
Thus, if the end-diastolic volume of the ventricle is increased, as can happen with bradycardia, in
the supine position, or during hand grip or squatting, the S1 -prolapse interval is increased.
Similarly, if the end-diastolic volume is decreased, as can occur in tachycardia, upon standing up,
and during the Valsalva maneuver, the S1 -click interval decreases. This time-based variation can
help identify the click of mitral or tricuspid prolapse from other heart sounds.