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Memahami dan menjelaskan macam – macam kedaruratan
kardiovaskuler
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Cardiac Emergencies• Acute Coronary Syndrome
– Acute Myocardial Infarction (Coronary Occlusion)
– Complications of Myocardial Infarction• Shock• Congestive Heart Failure• Acute Mitral Regurgitation &
Ventricular Septal Rupture• Myocardial Rupture• Systemic or Pulmonary Embolization• Pericarditis
– Angina pectoris• Heart Failure
– Severe Heart Failure– Mild to Moderate Heart Failure
• Hypertension & Hypertensive Crisis
• Pericarditis, Pericardial Effusion, & Cardiac Tamponade– Pericarditis & Pericardial Effusion– Cardiac Tamponade
• Myocarditis & Cardiomyopathy• Aortic Aneurysms & Dissections• Congenital Heart Disease
– Cyanosis– Anoxi Spells– Heart Failure– Pulmonary Hypertension– Coarctation of the Aorta
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Acute Myocardial Infarction
• Clinical findings :– Signs and Symptoms• Chest discomfort ( substernal and may radiate to
neck/left arm.• Occasionally (right arm, shoulders, back, or
epigastrium.• Squeezing oppressive pain characteristic.• Anxiety, restlessness, nausea, vomiting, abdominal
bloating, dyspnea, diaphoresis• S4 gallop / S3 gallop
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Acute Myocardial Infarction
– Electrocardiographic Findings :• High-voltage T waves, elevated ST segments, ST-
segment-elevation myocardial infarction, abnormal Q waves.• T wave inversion (some patient).• NORMAL ECG DOESN’T RULE OUT THE POSSIBILITY OF
MYOCARDIAL INFARCTION.
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Acute Myocardial Infarction– Laboratory Findings :
• CK-MB– Elevate : 4-6 hr after onset– Peak : 12-24 hr after onset– Return to baseline : 2-3 days after
onset• Troponin
– Elevate :2-6 hr after onset– Peak : 12-24 hr after onset– Stay elevated : 7-10 days
• Myoglobin– Elevation : 1-3 hr after onset– Peak : 4-12 hr after onset– Stay elevated : 12-36 hr after onset
– Differential Diagnosis• Aortic dissection• Pericarditis• Gastronintestinal
disorders
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Acute Myocardial Infarction– Treatment :
• Immediate :– IV infuse 0.9% NS– Oxygen 2-5L/min– ECG monitoring– + chest pain nitroglycerin 0,5 mg
» Repeat in 5 minutes if not working» Chest pain + BP >100 mmHg IV nitroglycerin 10 μg/min
and increase 5μg/min every 3-5 min until BP -10% or chest pain relieved.
– Narcotic analgesic (persistent chest pain)– Furosemide 40 mg bolus pulmonary edema– Β-blockers : 5mg metoprolol in 3 5-mg IV at 2 minutes intervals.
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Acute Myocardial Infarction– Treatment :
• Additional :– CBC– Serum creatinine– Electrolyte measurements– Blood urea nitrogen determinations– Enzyme levels– Platelet count– Prothrombin time– Ptt
• Option 1 : thrombolytic therapy• Option 2 : PCI
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Complications of Myocardial Infarction
• Shock– Disebabkan oleh :
• Penurunan cardiac output• Aritmia• Hipovolemia• Infark ventrikel kanan• Ruptur septum ventrikel• Regurgitasi mitral
– Clinical findings :• Hipotensi • Kebingungan• Rasa lelah• Kulit dinginn• Oliguria• Asidosis metabolik
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Complications of Myocardial Infarction
– Treatment :• Airway management
– Oxygen 5-10 L/min• Venous Pressure Management
– Swan-Ganz pulmonary artery catheter• Other measures
– Fluid exchange– Correct arryhtmia
• Drug Therapy– Dobutamine 2,5-20 μg/kg/min
• PCI
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Congestive Heart Failure
– Disebabkan oleh :• Infark miokard luas• Overload volume• Aritmia• Rergurgitasi mitral akut• Ruptur septal ventrikel
– Clinical Findings• Dyspnea• Takipnea• Takikardi• Edem paru• Distensi vena jugularis• Hipoxemia
– Treatment :• Airway management
– 5-10 L/min oxygen
• Drug therapy – Furosemide 40 mg
bolus IV– Morphine 2-8 mg IV– Nitroglycerin ointment
1,25 cm-2,5cm
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Angina
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ANGINA PECTORISDefinisi : nyeri dada sementara atau suatu perasaan tertekan, yang terjadi jika otot jantung mengalami kekurangan oksigen akibat pembuluh darah yang menyempit.
Angina terjadi bila penyumbatan blok telah mencapai 70 persen atau lebih. Biasanya penyumbatan disebabkan oleh lemak.
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• Nyeri angina dapat menyebar ke lengan kiri, ke punggung, ke rahang atau ke daerah abdomen.
• Penyebab angina pektoris adalah suplai oksigen yang tidak adekuat ke sel-sel miokardium dibandingkan kebutuhan.
• ETIOLOGI : sumbatan, spasme atau penyempitan arteri coronaria (ateri yg
memperdarahi jantung)
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KLASIFIKASI ANGINA PECTORIS
Dibagi menjadi 4 :• Stable angina pectoris • Unstable angina pectoris • Angina variant • Angina mikrovaskular
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STABLE ANGINA PECTORIS
• Etiologi : stenosis arteri koroner karena aterosklerosis kebutuhan metabolik otot jantung dan energi tidak dapat dipenuhi
• Keluhan nyeri dada akan timbul bila melakukan suatu pekerjaan.
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UNSTABLE ANGINA PECTORIS
• Etiologi : kontraksi otot polos pembuluh koroner iskemia miokard.
• Patogenesis spasme tersebut hingga kini belum dapat diketahui, kemungkinan tonus alphaadrenergik yang berlebihan.
• Manifestasi pembuluh koroner yang paling sering adalah variant (prinzmental).
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PATOFISIOLOGI ANGINA PECTORIS
Faktor-faktor Resiko(dislipidemia, genetik, sedentary lifestyle, alkoholisme,
usia, jenis kelamin, obesitas, dll)↓
Atherosklerosis pada arteri koronaria ↓
Suplai darah ke jantung ber<<↓
Iskemia↓
Hipoksia ↓
Angina Pectoris
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• GEJALA KLINIS : – Letak :
Daerah sternum, substernal, atau dada sebelah kiri–Kadang menjalar ke lengan kiri, punggung,
rahang, leher, atau ke lengan kanan–Nyeri dada juga dapat timbul di daerah
epigastrium, leher, rahang, gigi, bahu– Jarang terlokalisasi di bawah umbilikus atau
di atas mandibula).
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• Kualitas – nyeri dada biasanya seperti tertekan benda berat,
seperti diperas, atau terasa panas• Hubungan dengan aktivitas – biasanya timbul pada saat melakukan aktivitas– Kasus berat aktivitas ringan menimbulkan nyeri
dada, hilang bila menghentikan aktivitasnya. • Serangan angina dapat timbul pada waktu istirahat atau
pada waktu tidur malam. • Lamanya serangan – Biasanya berlangsung 1-5 menit– Bila nyeri > 20 menit infark miokard akut
• Keluhan lain : sesak napas, perasaan lelah, kadang-kadang nyeri dada disertai keringat dingin
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DIAGNOSIS & DIAGNOSIS BANDING
Sakit di dada dapat disebabkan oleh berbagai struktur, termasuk jantung, paru, pericardium, pleura, kelainan pembuluh darah besar, mediastinum, esophagus, dll. Kelainan neuromuskular dan muskuloskeletal juga dapat menimbulkan nyeri.
Evaluasi dimulai oleh 5 pertanyaan:› Di mana sakitnya? (lokasi)› Seperti apa sakitnya? (sifat)› Apa penyebabnya? (sebab/pencetus)› Ke mana menjalarnya? (radiasi)› Apa yang mengurangi sakitnya? Apa yang anda lakukan
bila sakitnya datang? (bebas sakit)
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DIAGNOSIS & DIAGNOSIS BANDING
Rasa sakit yang khas adalah retrosternal. Radiasi dapat menyebar ke:
› Leher (perasaan tercekik).› Bagian dalam tangan kiri di bawah ketiak
(bandingkan dengan sakit dari muskuloskeletal yang biasanya di bahu atau di luar tangan)
Sifat sakitnya seperti tertekan, perasaan kencang atau berat, seperti diperas, sesak, atau pegal. Perasaan seperti ditusuk pisau biasanya bukan infark miokard.
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DIAGNOSIS & DIAGNOSIS BANDING
PERBEDAAN SIFAT SAKIT DADA
JANTUNG NON-JANTUNG
Tegang tidak enak Tajam
Tertekan Seperti pisau
Berat Ditusuk
Mengencangkan / diperas Dijahit
Nyeri / pegal Ditimbulkan tekanan / posis
Menekan / menghancurkan Terus menerus seharian
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CARDIAC ARREST
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CARDIOVASCULAR COLLAPSE
Cardiovascular collapse : hilangnya aliran darah efektif akibat disfungsi jantung atau pembuluh darah perifer akut.Kausa :
vasodepressor syncope (vasovagal syncope, postural hypotension with syncope, neurocardiogenic syncope)transient severe bradycardiacardiac arrest
Cardiovascular collapse bersifat transient, kecuali cardiac arrest.
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CARDIAC ARREST
Cardiac arrest : terhentinya fungsi pompa jantung yang memerlukan tindakan untuk mengembalikan fungsi tersebut.
Mekanisme elektrik pada cardiac arrest :Ventricullar fibrillation (50-80%)Bradiaritmia berat persistenAsistolPulseless electrical activity (PEA; an organized electrical activity without mechanical response)Ventricular tachycardia (VT)Cardiac output ↓ e.c. PE masif akut, aneurisma aorta, reaksi anafilaksis, dan tamponade pasca MI.
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Etiologi Cardiac Arrest
STRUCTURAL CAUSES Coronary heart disease (>80%) Coronary artery abnormalities Myocardial infarction
Myocardial hypertrophy Dilated cardiomyopathy—primary muscle disease Inflammatory and infiltrative disorders Valvular heart disease Electrophysiologic abnormalities, structural Inherited disorders of molecular structure associated with electrophysiologic abnormalities (e.g., congenital long QT syndromes, Brugada syndrome)
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ETIOLOGI CARDIAC ARREST
Iskemia koroner akutPenyebab henti jantung di 50% kasusIritabilitas miokard menyebabkan fibrilasi ventrikel (VF)
Disritmia primer :Abnormalitas elektrik kongenital atau didapatHipertrofi/ dilated cardiomyopathyMiokarditis
Ruptur jantung
Tamponade jantung
Abnormalitas metabolik
ETIOLOGI CARDIAC ARREST NON-CARDIAC
Pikirkan terutama pada kasus PEA
Tension pneumothorax
Perdarahan
PE masif
Sepsis
Asidosis berat
Obat : anti-aritmia, digoxin, beta-blocker, CCB, tricyclic antidepressant, cocain, heroin
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Faktor Kontributor CA
FUNCTIONAL CONTRIBUTING FACTORS Alterations of coronary blood flow Transient ischemia Reperfusion after ischemia
Low cardiac output states Heart failure (chronic, acute decompensation) Shock
Systemic metabolic abnormalities Electrolyte imbalance (e.g., hypokalemia) Hypoxemia, acidosis
Neurophysiologic disturbances Autonomic fluctuations : central, neural, humoral
Toxic responses Proarrhythmic drug effectsCardiac toxins (e.g., cocaine, digitalis intoxication)Drug interactions
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Karakter Klinis Cardiac Arrest
PRODROMAL ONSETAnginaDyspneaPalpitasiMudah lelah
Gejala tidak spesifik untuk cardiac arrest.
: perubahan status kardiovaskular akut yang dapat menimbulkan cardiac arrest dalam waktu 1 jam.EKG : perubahan aktivitas elektrik (VF, VT)Kesuksesan resusitasi bergantung pada interval waktu antara onset & tindakan intervensi.
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Tanda & Gejala
Tidak responsifTidak ada pulsasi nadiPernapasan dangkal & terengah selama beberapa menit
Biasanya disertai :Sakit dada
DyspneaPalpitasiKejang
Segera setelah henti jantung terjadi :Shock atau hipotensiGangguan status mental
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Diagnosa Banding
Hilang kesadaran mendadak dengan pulsasi teraba :SyncopeSeizureAcute strokeHypoglycemiaAcute airway obstructionHead traumaToxins