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cor pulmonale
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COR PULMONALE
Dr. S.E.E. Palupi Sp.JP
Cor Pulmonale chronicumHipertrofi dilatasi ventrikel kanan akibat hipertensi pulmonal yg diakibatkan oleh :•Penyakit paranchym paru.•Penyakit sistem vaskuler dari MPA – V. Pulmonalis.•Kelainan dinding thorax•Kelainan ventilasi paru•Kelainan dinding thorax.Disingkirkan :
Disfungsi ventrikel kanan (RV) akibat gagaljantung kiri.Congenital HD.M.S
• Cor pulmonale akutMeningkatnya beban R.V. secara akut akibat :Hipertensi pulmonal akut akibat emboli pulmonal pd thrombo emboli
Perjalanan Penyakit
Gagal jantung kanan dapat terjadi akut pd DVT (Deep Vein Thrombus emboli lepas
A. Pulmonalis dan cabang-cabangChronic : P.P.O.K.Akut on chronic : P.P.O.K dng infeksi atau
hypoxia beratUS 20% pend. Dng gagal jantung : C.Pulm.INDONESIA ? Insiden perokok
polusi
Fungsi Sirkulasi Pulmonal (normal)
• Pertukaran gas• Membuang particles• Konversi AI AIIRespiratory movement (bernafas)
memfasilitasi aliran darahInsp venous return Exp Peredaran sistemik
Stroke Volume R.V (= LV) tergantung :
• Preload• Kontraktilitas• Afterload• Patofisiologi :• Kenaikan afterload hypertrophy dan
dilatasi R.V.
Sebab-sebab Kenaikan Afterload• Hiper inflasi pd PPOK kompresi kapiler alveoli,
memanjangnya pembuluh darah paru.• Volume paru berkurang : post reseksi paru yg
luas. Penyakit paru restriktif kompresi dan distorsi pembuluh darah paru
• Hipoxia vasokontriksiHipertensi pulmonal
• Hipoxia Hematocrite • viskositas darah hipertensi pulmonal
A. Penyakit Vaskuler Paru
(Cor Pulm. Akibat penyakit vaskuler paru chronic)•Emboli pulm berulang•Recurrent medium sized emboli yg tdk mengalami lysis, organized chronic thrombo embolic pulm. hypertension.•Partikel yg berasal IVDA, metastase tumor.•Pulm. vasculitis•Pulm vasoconstriction pd dataran tinggi.•Primary Pulm. Hypertension.
Manifestasi Klinis :
• Dysp + tachypnea – Hip. Pulm.e.c. vasc.• Exercise dan istirahat• Tidak berkurang pd posisi duduk• Batuk tdk produktif• Chest pain : Dilatasi A. Pulmonalis atau
Ischemia R.V.• Hepatomegali, udema tungkai• Cyanosis : hypoxemia arterial atau
CO• R.V kuat angkat – para sternal kiri atau
epigastrium
• Ejection click• P2 keras• Proto diastolic gallop (S3), (S4)• Pan syst. Murmur ec TR.• JVP hepoto jugular reflux +• Kelainan fisik akibat R.V. failure dpt
berkurang/hilang apabila tekanan A. Pulmonalisdng menurunkan keadaan hipoxia
Laboratorium• Radiologi : A. Pulm. Dan cabang-cabang
dilatasi• Right Desc.Pulm. A>.• Adanya DVT menetapkan diagnosa Pulm.
Vasc. Disc (Vacular Doppler)• EKG : P.Pulmonale
– RVH– RAD– Aritmia – (mungkin)
• Echo : - Pengukuran tebal dinding RV - Dilatasi RV dibanding LV.
IVS : terdorong ke kiriMRI : mengukur massa RVMyocardial perfusion scintigraphyThallium scanningSestamibi RVH dpt diterapkan Normal : RV”is not imaged” uptake LV sangat
besarKateerisasi jantung
Tekanan vaskuler paruLung biopsi vaskulitis, dsb
II. Acute Cor Pulmonale akibat
Emboli massive atau MultipleAcute R.V failure akibat emboli paru massive
dicurigai pd hal sebagai berikut:• Sudden onset of severe dyspnoe• Cardio vascular collaps pd penderita dng
venous thrombosis.
Manifestasi Klinis Acute R.V. Failure
• Pucat • Berkeringat• Hypotension• Rapid pulse, small amplitude• Neck vein : distended.
V. wave nyata/ TR.• Hepatomegali : lunak
Nyeri tekanPulsatile
• Pan SM – TRPunct max : para sternal kiri
• S4 gallop• A.G .D : PO2 (Kegagalan ventilasi-perfusi)
PCO2 (hiperventilasi)
Terapi V.T.E.• LMWHMempunyai kelebihan dibanding unfractionated heparin :Tak perlu monitoring laboratorium (APTT)Pemberian s.c.Bio availability lebih tinggiPlasma half life lebih lamaL.O.S lebih pendek• UF heparinBolus : 60 – 70 U/kg, BB : max 5000 U.Dilanjutkan dengan:12 – 15 U/kg/jam max : 1000 U/jam.APTT 1,5 – 2,5 ><1controlHitung thrombocyt : mewaspadai induced
thrombocytopenia
• Oral anticoagulant (warfarin)3 – 6 bulan : reversible VTE:SurgeryTraumaPemakaian estrogen≥6 bulan : idiofathic12 bulan : - life time :Anti thrombin deficiency.• Obat-obat inotropicDobutamine infuse :Dosis : 2,5 – 10 mcg/kg/menitTitrasi : berdasar respon terhadap H.R.C.OUrine output
IndikasiTanda-tanda CO (vasocontriction) tetapi tekanan darah masih baik (SBP≥ 90 mmHg.Dopamine infuse:Dosis : 2,5 – 10 mcg/kg/menit
Titrasi berdasar : H.R, CO, Urine output
•O2Inhalasi : O2 100% menurunkan R.V
Afterload•Terapi thrombolyticIndikasi : massive P. embolism.Kontraindikasi : absolute
relative
Absolute C.I1. Active internal bleeding2. Recent spontaneous intra cranial bleedingRelative C.I1. Major surgeryDeliveryOrgan biopsyPuncture of a non compressible vessel in the preceding
10 days.2. IschStroke – 2 mo3. G.I bleeding – 10 days.4. Serious trauma – 15 days.5. Neuro surgery w/in 1 monthOpthalmic surgery
6. Uncontrolled severeHypertensionSBP ≥ 180 mmHg, DBP ≥ 110 mmHg7. Recent CPR8. Platelet count < 100.000/ml9. Pregnancy10. Bacterial endocarditis11. Diabetic hemorrhage retinopathy.Streptokinase :250.000 i.u IV loading dilanjutkan dengan100.000 i.u/jam – 24 jamTerapi thrombolytic diharapkan berhasil dng fragmentasi
embolus dan tekanan menurun cepat
ACUTE COR PULMONALE
Thrombi in right heart (septal infarction, atrial fibrillation)
Tumor emboli
Air emboli
Pelvic-vein thrombi (following pelvic or prostatic surgery)
Fat emboli (fractures)
Thrombi in deep veins of lower extremity
Multiple emboli in pulmonary arterial tree with acute infarcts
Massive emboli of pulmonary trunk and main pulmonary arteries without infarction; right heart dilated
Thrombus in Left common, external, and internal iliac
veins, loosely attached to the vessel wall; A common
source of pulmonary emboli
B. Cor Pulmonale Akibat Penyakit Parenchym Paru
Cor. Pulm. Pd PPOK menunjukkan prognosis yg kurang baik. Penyebab tersering PPOK.
Masalah Hipertensi Pulm pd PPOK
1. Pulm. Vasocontriction akibat hypoxiaStimuli menyebabkan Penebalan tunica media A. Pulm dan cabang-cabang.
2. Hilangnya pembuluh darah kecil, pd tempat emphysema, jaringan paru yg rusak.
3. Kenaikan CO & viskositas darah akibat polycythemia akibat hypoxia.
4. PPOK chronic hypoxia disfungsi LVtekanan LA
Tekanan A. PulmonalisDisfungsi LV akibat isch. Myocard pd perokok.
5. RV. FailureRV failure merupakan komplikasi cor pulmonale.Dicetuskan : gagal nafasInfeksi jalan nafasHipertensi pulm.6. Aritmia supraventricular dan atauVentricular7. Hepatomegali : lunak (palp)Tepi tumpulLicinHJR reflux +8. Udema perifer.Eksaserbasi obstruksi jalan nafas oleh infeksi tekanan
intrathoracic venous return udema perifer.9. Bendungan vena sistemik akibat obstr jalan nafas dpt menurun
apabila berkurangnya/ hilangnya obstr atau infeksi
Patologi Anatomi RVH, MPA dilatasi. Tunica media cabang-cabang A. Pulm menebal,
fibrosis, elastisitas sampai ke arteriole berkurang. Kapiler: Distorsi. dan Menghilang pd tempat-tempat Terjadi hiperinflasi paruManifestasi Klinis.Riwayat batuk produktifSesak nafas membatasi aktivitasRiwayat perawatan RS akibat ;Infeksi jalan nafasMech ventilation selama perawatanHypoxia pd malam hari akibat hypoventilation.
Pemeriksaan Fisik• Nicotine staining• Kulit hangat• Arterial pulse• Distensi thorax• Rhonchi +• Wheezing akibat bronchitis chs• S3 gallap dari RV• Pan SM TR• Udema perifer• Kenaikan systemic venous pressureAF, infeksi pulmonal.• Hepatomegali ; HJR (+) JVP
LaboratoriumFungsi pulmonal menurunFoto thoraxAkibat hiperinflasiPembesaran R.V sukar ditentukan MPA : dilatasi ke periferHilangEKG : Kurang peka menunjukkan RV hiperinflasi paru
konduktor buruk utk impuls listrik Aritmia:Echo : hipertrofi RV Dilatasi RVMyocardium perfusion scintigraphy RV uptake tinggi
Kateterisasi :Pulm. Artery Wedge Pressure masih mungkin normal
apabila tdk ada komplikasi.Theraphy.Harus optimal.Infeksi jalan nafas akibat akut yg dpt merupakan pemicu
RV failure. Harus segera diobati dan adequate.Memperbaiki ventilasiObstruksi diperbaikiO2 ditambahLong term O2 therapy dpt menelong penderita PPOK
tekanan A. Pulm.Broncho dilator dan A.B memperbaiki obstr jalan nafas.
Diuretica : Menghilangkan udemaIngat : venous return dan CODigitalis : RV failure.Mudah intoxicatie pd keadaan HypoxiaPhlebotomy : apabila Ht > 55 %Inhalasi NO – dlm evaluasi
C. Cor Pulm. Akibat Penyakit Paru RestrictiveObliterasi vascular bed.D. Cor Pulm. Akibat kelainan Vantilasi :• Neuromusc apparatus• Chest wall• DiaphragmaMech : Hypoxia chronicTertekannya cabang-cabang A. Pulm
E. Cor Pulm. Kel. Kontrol PernafasanSleep apneaObstruksi jalan nafas atasF. Cor Pulm. Pd KetinggianHypoxia chronic sec polycythemiaHipertensi Pulm.
Cor Pulm.Turun kedataran rendah
Hypoxia atau (-)
CHRONIC COR PULMONALE
Extensive pulmonary emphysema with great distention of pulmonary trunk and main pulmonary arteries which have pressed the aorta against the trachea; pulmonary arteriosclerosis and right ventricular hypertrophy
Hypertrophy and dilatationof right ventricle
X-Ray : Chronic obstructive emphysemawith cor pulmonale
R waves in leads V1 and V2 as well as S waves in leads I, V4, V5, and V6 are indicative of right ventricular hypertrophy; prominent P waves in leads II, III, aVF, V1 and V2 suggest right atrial enlargement
CHRONIC COR PULMONALE
Chronic Lung Disease
Reduction in pulmonary vascular bed
Acidosis and hypercapnia
Pulmonary hypertension
Polycythemia andhyperviscosity
Hypertrophy and dilatation of the right ventricle
Right ventricle failure
Hypoxia
WR Summer, in LJ Rubin (cd): Pulmonary Heart Disease, Boston, Martinus Nijhoff, 1984, P 285
Pathogenesis of Cor Pulmonale
Mechanism Responses Characteristic
RESPIRATORY DISEASE
Obstructive
Chronic bronchitis and emphysema : chronic asthma
Pulmonary hypertension due to hypoxia, vascular stretching, and loss of vessels. Heart beat impeded externally by lung hyperinflation. Normal or high output
Chronic cor pulmonale “Blue bloater” or “Pink puffer”
Restrictive
1. Intrinsic : interstitial fibrosis lung resection
Hypertension due to hypoxia, vascular distortion and loss.
Chronic cor pulmonale
Breathlessness
Hyperventilation
2. Extrinsic : obesity, myedema, muscle weakness, kyphoscoliosis, upper airway obstruction, diminished respiratory drive, high altitude
Normal or low output. Hypertension due to alveolar hypoxia.
Chronic cor pulmonale
Peripheral edema
Hypoventilation
Cor Pulmonale
Mechanism Responses Characteristic
PULMONARY VASCULAR DISEASE
Emboli, large or multiple Fall in cardiac output due to acute obstruction
Acute cor pulmonale, right ventricular distention, shock
Emboli, small ; vasculitis ; widespread lung damage (ARDS)
Pulmonary hypertension due to widespread hypoxia and microvascular obstruction
Subacute cor pulmonale, right ventricular distention, breastlessness and fever
Emboli, medium, and recurrent; Primary pulmonary hypertension; diet or drug vasopathy
Pulmonary hypertension due to vascular obstruction
Low or normal cardiac output
Chronic cor pulmonale
Right heart hypertrophy
Breathlessness
Note : ARDS = Acute respiratory distress syndrome