10_sixthproblem.pptx

th 6

Problem Emergency Medicine Block Group 10 October 29th, 2018

Group member Tutor: dr. Agus Ketua : Kurnia Elsa Oktaviana Sekretaris : Erika Juniartha Tungki Penulis : Marshally Safira Masrie Anggota: • Maria Meilani Christina • Elfinder Singh Dhillon • Stevanno Geraldus • Merlyn Priscilla • Timmy Yonatan Nangoy • Clareta Vero Patricia W • Irwan Surya Angkasa • Thalia Christabel

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The dangerous heartbeat A 60-year-old man came to the Emergency Department with severe chest pain extending his jaw and left arm. He suddenly felt the chest pain 3 hours ago while he was watching television, accompanied by excessive cold sweat, nausea, and vomiting. He alse felt shortness of breath since an hour ago. He has a history of hypertension, diabetes mellitus, and hypercholesterolemia in the past 3 years. He is not taking his medication regularly, has been smoking since the last 10 years and never exercises. Previously, he had suffered an episode of mild chest pain but the symptom disappeared after resting. No history of stroke in the past. physical examination result: compos mentis (GCS 15), looks in pain, agitated, overweight and having mild-dyspnea. Blood pressure 170/90 mmHg, heart rate 120 beats per minute (regular with enough volume and firmness), respiratory rate 30 breaths per minute (slow and superficial), afebrile and slight increase in JVP. Inspection, palpation, and percussion of the heart are in normal limits; S1 & S2 in heart auscultation are normal, no murmur is found. Inspection, palpation, and percussion of the lungs are in normal limits but fine rales at the basis of the lung can be heard in auscultation. Abdomen examination is normal. His extremities are warm. The image below is his 12 lead ECG result: A few moments later, he suddenly experiences a seizure and falls unconscious. His ECG monitor result is shown on the image below: Identify the problems in this case chronologically, discuss the problems and plan the proper treatment while considering all possibilities!

Mind map Cardiovascular Emergency

Non-cardiorespiratory arrest

Cardiorespiratory arrest

Acute Coronary Syndrome

Diseksi aorta

Acute cor pulmonale Supraventrikular takikardi

Aritmia

Ventrikular takikardi

Acute cardiac failure Ventrikel fibrilasi

Angina pectoris

Miokard infark

Unstable angina pectoris

STEMI

NSTEMI

Learning issues 1. Menjelaskan klasifikasi cardiovascular emergency 2. Menjelaskan Definisi, Etiologi, Tanda & Gejala, Diagnosis (PF & PP), Tatalaksana Awal, Komplikasi, serta Prognosis

Klasifikasi cardiovascular emergency LI 1

Cardiovascular Emergencies 1. Tidak sadar Cardiac Arrest - Ventricular Fibrillation / Pulseless Ventricular Tachycardia - Asystole - Pulseless Electrical Activity (PEA)

2. Sadar Acute Coronary Syndrome (ACS) - Oklusi parsial: Unstable Angina Pectoris (UAP) & Acute Non ST-Elevation Myocardial infarction (NSTEMI) - Oklusi total: Acute ST-Elevation Myocardial infarction (STEMI) Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011

ETIOLOGI

ETIOLOGI ATEROSKLEROTIK

Thrombosis arteri koroner Coronary emboli from mechanical or infected cardiac valves

NON ATEROSKLEROTIK

Inflammation from acute vasculitis

Connective tissue disorders Peripartum women (spontaneous coronary artery dissection)

Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011

Menjelaskan Definisi, Etiologi, Tanda & Gejala, Diagnosis (PF & PP), Tatalaksana Awal, Komplikasi, serta Prognosis 1. 2. 3. 4. 5.

Angina pectoris Acute cor pulmonal Miokard infark Ventrikular takikardi Supraventrikular takikardi

6. 7. 8. 9.

Ventrikular fibrilasi Cardiorespiratory arrest Acute cardiac failure Diseksi aorta

Angina pectoris

Angina Pectoris :Angina tidak stabil apabila pasien mempunyai keluhan iskemia sedangkan tidak ada kenaikan dari serum biomarkers. • Perbedaan angina tidak stabil dengan NSTEMI miocard infark menurut pedoman American Heart Collage of Cardiology (ACC) dan America Heart Association (AHA) ialah apakah iskemia yang timbul menyebabkan kerusakan pada miokardium sehingga adanya pertanda kerusakan miokardium yang dapat diperiksa. Buku Ajar Ilmu Penyakit Dalam Ed VI

Angina Pectoris: Patogenesis • Ruptur plak arterosklerosis merupakan penyebab tersering. Sehingga secara tiba – tiba terjadi oklusi subtotal atau total dari pembuluh darah koroner yang sebelumnya mempunyai penyempitan yang minimal. • Terjadinya ruptur  aktivasi, adhesi, dan agregasi platelet  aktivasi terbentuknya trombus. • Bila trombus menutupi 100% lumen pembuluh darah  infark dengan ST segmen elevasi. • Bila trombus tidak menurupi 100% dan hanya menimbulkan stenosis  angina tidak stabil.

Buku Ajar Ilmu Penyakit Dalam Ed VI

Angina Pectoris: Manifestasi klinis • Keluhan pasien umumnya angina untuk pertama kali atau keluhan angina yang lebih berat dari biasanya. • Nyeri dada pada angina dapat timbul pada saat istirahat atau timbul pada aktivitas yang minimal. • Nyeri dada dapat disertai: • Sesak napas • Mual dan muntah • Kadang disertai keringat dingin.

Buku Ajar Ilmu Penyakit Dalam Ed VI

Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011

Angina Pectoris: Pemeriksaan • EKG (elektrokardiografi): • Pemeriksaan EKG sangat penting untuk menegakkan diagnosis. • Adanya ST segmen depresi menujukkan kemungkinan adanya iskemia akut. • Gelombang T negatif juga merupakan pertanda iskemia atau NSTEMI. • Perubahan gelombang ST dan T yang nonspesifik seperti depresi segmen ST < 0.5 mm dan gelombang T negatif < 2mm, tidak spesifik untuk iskemia, dan dapat disebabkan karena hal lain.

Buku Ajar Ilmu Penyakit Dalam Ed VI

• Uji latih: • Pasien yang telah stabil dengan terapi medikametosa dan menunjukkan tanda resiko tinggi perlu pemeriksaan exercise test dengan alat treadmill. • Bila hasilnya negatif prognosis baik • Bila hasil postifi dan didapatkan adanya depresi segmen ST yang cukup dalam, dianjurkan untuk melakukan pemeriksaan angiografi koroner untuk menilai kedaan pembuluh koroner apakah perlu dilakukan tindakan revaskularsisasi.

• Ekokardiografi: • Pemeriksaan ini tidak memberikan data untuk diagnosis angina tidak stabil secara langsung.

Angina Pectoris: Pemeriksaan Laboratorium • Pemeriksaan troponin T atau I dan CK – MB merupakan pertanda paling penting dalam menegakkan diagnosis. • Menurut European Society of Cardiology (ESC) dan ACC dianggap mioknekrosis bila troponin T atau I positif dalam 24 jam. Troponin tetap positif sampai 2 minggu. • CK – MB kurang spesifik untuk diagnosis karena juga ditemukan di otot skeletal, tapi berguna untuk diagnosis infark akut dan akat meningkat dalam beberapa jam dan kembali normal dalam 48 jam. Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011 Buku Ajar Ilmu Penyakit Dalam Ed VI

Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011

Angina Pectoris: Tatalaksana

Source : Toronto. Essential med notes 2015.

Angina Pectoris: Komplikasi

Acute cor pulmonale

Acute cor pulmonale • Right ventricular hypertrophy (RVH) or dilation caused by elevated pulmonary artery pressure. • RVH due to a systemic defect or congenital heart disease is not classified as cor pulmonale.

• Acute cor pulmonale: • Right ventricle is dilated & muscle wall stretched thin • Overload due to acute pulmonary hypertension (HTN) • Most often caused by massive pulmonary embolism

• Chronic cor pulmonale: • RVH with eventual dilation and rightsided heart failure • Caused by an adaptive response to chronic pulmonary HTN • Predominately occurs as a result of alveolar hypoxia

• Etiologi: • • • • • • • • • • • • • • • • •

Chronic hypoxia COPD High-altitude dwellers Sleep apnea Chest deformities Kyphoscoliosis Pulmonary embolism Interstitial lung disease Scleroderma Systemic lupus erythematosus Mixed connective tissue disease Sarcoidosis Pulmonary Langerhans cell histiocytosis Neurofibromatosis Lymphangioleiomyomatosis Cystic fibrosis Severe anemia

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health

• Obesity • Pulmonary veno-occlusive disease • Pulmonary vascular obstruction secondary to tumors or adenopathy • Increased blood viscosity: • Polycythemia vera • Leukemia • Increased intrathoracic pressure: • Mechanical ventilation with positive end-expiratory pressure • Idiopathic primary pulmonary HTN

Acute cor pulmonale: manifestasi klinis • Tanda dan gejala: • • • • • • • • • • • • • • •

Exertional dyspnea Easy fatigability Weakness Exertional syncope Cough Hemoptysis Exertional angina even in the absence of coronary disease Anorexia Right upper quadrant discomfort Wheezing Hoarseness Weight gain Hepatomegaly Ascites Peripheral edema

End-stage cor pulmonale • • • •

Cardiogenic shock Oliguria Cool extremities Pulmonary edema secondary to intraventricular septum impairing left ventricular diastolic function

• Riwayat: • • • • • •

Exercise intolerance Palpitations Chest pain Lightheadedness Syncope Swelling of the lower extremities

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health

• Physical-Exam • • • • •

Jugular venous distention Prominent A- and V-waves Increase in chest diameter Crackles and/or wheezes Left parasternal heave on cardiac palpation • Splitting of the 2nd heart sound or murmurs of the pulmonary vasculature may be heard. • Hepatojugular reflex and pulsatile liver • Pitting edema of the lower extremities

Acute cor pulmonale: Pemeriksaan Laboratorium: • Pulse oximetry or ABG: • Resting PO2 40–60 mm Hg • Resting PCO2 often 40–70 mm Hg

• Hematocrit: • Frequently elevated

• B-natriuretic peptide: • When elevated, is sensitive for moderate to severe pulmonary HTN, and may be an independent predictor of mortality • Elevated level alone is not enough to establish diagnosis of cor pulmonale. Other lab tests are not generally useful.

1. CXR: Signs of pulmonary HTN: • Large pulmonary arteries (>16–18 mm) • An enlarged RV silhouette • Pleural effusions do not occur in the setting of cor pulmonale alone.

2. Echocardiography • The noninvasive diagnostic method of choice • RV dilation or RVH • Assessment of tricuspid regurgitation

3. Chest CT, ventilation/ perfusion scans, or pulmonary angiography: • Useful in the setting of acute cor pulmonale

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health

3. MRI • Superior to echocardiography for assessment of right ventricular size & function

4. Pulmonary function tests • Impaired diffusion capacity due to pulmonary HTN

5. Right-heart catheterization: • The most precise estimate of pulmonary vascular hemodynamics • Gives accurate measurements of pulmonary arterial pressure and pulmonary capillary wedge pressure

Acute cor pulmonale: Pemeriksaan & DD 6. EKG: • Right-axis deviation

• Small R-waves and deep S-waves across the precordium

DIFFERENTIAL DIAGNOSIS

• Right bundle branch block

• Right atrial enlargement; Tall, peaked P-waves (P pulmonale)

• Primary disease of the left side of the heart

• RVH

• S1 Q3 pattern with acute cor pulmonale

• Mitral stenosis

• Dominant R-wave in V1 and V2

• Transient changes due to hypoxia

• Prominent S-wave in V5 and V6

• Congenital heart disease

• Right precordial T-wave flattening

• Eisen menger syndrome • Left to right shunt caused by a congenital heart defect in the fetal heart causes increased flow through the pulmonary vasculature, causing pulmonary HTN

• Hypothyroidism • Cirrhosis https://reference.medscape.com/features/slideshow/abnormalecg?pa=8nN9RPXta4tZ9RtmOofVGdBR4rzs%2FEqqnJ5hIz8dvPJ0JqBZYWZu%2Bl2yQYktlC1GJyGvMX%2Fu%2BWdIXoARf%2FT0zw%3D%3D

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health

Acute cor pulmonale: Tatalaksana PRE HOSPITAL

ED TREATMENT/PROCEDURES

Supportive therapy:

• Supplemental oxygen sufficient to raise arterial saturation to 90%:

• Supplemental oxygen  To an endpoint of 90% arterial saturation

• IV access • Cardiac monitoring • Pulse oximetry • Treat bronchospasm from associated respiratory disease: • β-Agonist nebulizers INITIAL STABILIZATION/THERAPY

• ED therapy is directed at the underlying disease process and reducing pulmonary HTN.

• Improving oxygenation reduces pulmonary arterial vasoconstriction and RV afterload. • The improved cardiac output enhances diuresis of excess body water.

• Care must be taken to monitor the patient’s ventilatory status and PCO2, as hypercapnia may reduce respiratory drive and cause acidosis.

• Diuretics: furosemide  added cautiously to reduce pulmonary artery pressure by contributing to the reduction of circulating blood volume: • Be wary of volume depletion and hypokalemia • Patients should be maintained on salt and fluid restriction. • There is no role for digoxin in the treatment of cor pulmonale.

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health

Bronchodilators:

MEDICATION

• Bronchodilator therapy is particularly helpful for those patients with COPD

• Furosemide: 20–60 mg IV • (peds: 1 mg/kg may increase by 1 mg/kg/q2h not to exceed 6 mg/kg)

• Selective β-adrenergic agents: terbutaline 0.25 mg SC may be useful.

• Bronchodilator affects and reduces ventricular afterload. • Theophylline may play a role to improve diaphragmatic contractility & << muscle fatigue. • Anticoagulation may be considered for those at high risk for • thromboembolic disease. • Acutely decompensated COPD patients: • Early steroid therapy • Antibiotic administration

In general, improvement in the underlying respiratory disease results in improved RV function.

• Terbutaline: 0.25 mg SC DISPOSITION • Admission Criteria • New-onset hypoxia • Anasarca: extreme generalized edema • Severe respiratory failure • Admission criteria for the underlying disease process • Discharge Criteria • Patients without hypoxia or a stable oxygen requirement • Issues for Referral • Close follow-up as long as the underlying etiology has responded to acute management • The need for a sleep study to assess for sleep apnea should be coordinated by the patient’s physician.

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health

Infark miokard

Zipes DP, Libby P, Bonow RO, Mann DL, Braunwald E. Braunwald’s heart disease: a textbook of cardiovascular medicine, 11th Edition. Philadelphia: Elsevier Inc.; 2019.

Infark miokard = nekrosis kardiomiosit akibat adanya iskemia miokard akut.

Kriteria: ↑/↓ biomarker kardiak (troponin) dengan ≥1:  Gejala iskemia  Perubahan gelombang ST-T atau left bundle branch block pada EKG  Gelombang Q patologis pada EKG  Imaging evidence  loss of viable myocardium or regional wall motion abnormality  Trombus intrakoroner yang terdeteksi dengan angiography atau autopsy

Zipes DP, Libby P, Bonow RO, Mann DL, Braunwald E. Braunwald’s heart disease: a textbook of cardiovascular medicine, 11th Edition. Philadelphia: Elsevier Inc.; 2019.

NSTEMI: Diagnosis Gejala Klinis • Nyeri angina: • Prolonged (>20 menit) nyeri angina saat istirahat • New onset (de novo) angina • Post-MI angina • Nyeri dada  sensation of pressure or heaviness (‘angina’) menjalar sampai lengan kiri, leher atau rahang yang dapat intermiten • Berkeringat, mual, nyeri abdomen, dispnea dan sinkop • Gejala atipikal  nyeri epigastrik, isolated dyspnoe (umum pada orang tua, wanita dan pasien DM, penyakit ginjal kronik, demensia)

ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. The European Society of Cardiology, 2015

o Eksaserbasi gejala setelah aktivitas fisik & membaik setelah istirahat o Kondisi presipitasi: anemia, infeksi, inflamasi, demam, kelainan metabolik atau endokrin (tiroid) Zipes DP, Libby P, Bonow RO, Mann DL, Braunwald E. Braunwald’s heart disease: a textbook of cardiovascular medicine, 11th Edition. Philadelphia: Elsevier Inc.; 2019.

NSTEMI: EKG

Dharma, S. Cara Mudah Membaca EKG. Jakarta: EGC; 2017.

ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. The European Society of Cardiology, 2015

NSTEMI: Algoritma manajemen

AHA/ACC Guideline for the management of patients with non ST-elevation acute coronary syndromes; 2014

NSTEMI: Komplikasi

GW Reed et al. The Lancet; 2017

STEMI Myocardial Infarction • AMI is defined as a clinical event involving myocardial ischemia in which there is evidence of myocardial injury. • Typically, this involves a rise and fall of cardiac biomarkers, w/ supportive evidence in the form of symptoms, suggestive electrocardiogram (ECG) changes.

• STEMI is a type of AMI with symptoms characteristic of myocardial ischemia associated with ST-segment elevation on the ECG. • It is defined Myocardial Infarction as new ST-segment elevation at the J point of at least two contiguous leads of : ≥2 mm (≥0.2 mV) in men or ≥1.5 mm (0.1 mV) in women in leads V2 and V3 or ≥1 mm in any other contiguous precordial leads or the limb leads for either gender. https://www.uscjournal.com/articles/st-segment-elevation-myocardial-infarction-challenges-diagnosis

STEMI: Diagnosis STEMI will typically result in intense pain or pressure in or around the chest, often radiating to the neck, jaw, shoulder, or arm. Profuse sweating, breathlessness, and a profound sense of impending doom also common. At times, the signs may be far less obvious, manifesting with nonspecific or generalized symptoms such as: • Pain around the shoulder blades, arm, chest, jaw, left arm, or upper abdomen • A painful sensation described as having a "clenched fist in the chest" • Discomfort or tightness in the neck or arm • Indigestion or heartburn • Nausea and vomiting • Fatigue or sudden exhaustion • Shortness of breath

• Dizziness or lightheadedness • Increased or irregular heart rate • Clammy skin https://www.verywellhealth.com/stemi-st-segment-elevation-myocardial-infarction-1746032

• In most cases, the diagnosis of STEMI can be made quickly once the person is under medical care. A review of symptoms, accompanied by the evaluation of the ST segment on the ECG, is usually enough for a doctor to begin treatment. • A review of cardiac enzymes may also help but usually arrives well after acute treatment is started. • It is important to stabilize the person as quickly as possible. • In addition to pain and distress, STEMI can cause sudden death due to ventricular fibrillation (a serious disturbance of the heart rhythm) or acute heart failure (when the heart cannot pump enough blood to properly supply the body).

• After a heart attack has run its course, the muscle itself may be left with substantial permanent damage. • Chronic heart failure is a common consequence of this, as is the increased risk of dangerous cardiac arrhythmias (irregular heartbeats ).

STEMI: Diagnosis Banding dan algoritma tatalaksana

https://www.uscjournal.com/articles/st-segment-elevation-myocardial-infarction-challenges-diagnosis

STEMI: Tatalaksana • Penatalaksanaan STEMI dimulai sejak kontak medis pertama, baik untuk diagnosis dan pengobatan.

Terapi reperfusi

• Diagnosis kerja infark miokard harus telah dibuat berdasarkan riwayat nyeri dada yang berlangsung selama 20 menit atau lebih yang tidak membaik dengan pemberian nitrogliserin.

• Terapi reperfusi segera, baik dengan IKP atau farmakologis, diindikasikan untuk semua pasien dengan gejala yang timbul dalam 12 jam dengan elevasi segmen ST menetap / Left Bundle Branch Block (LBBB) yang (terduga) baru.

• Diagnosis STEMI perlu dibuat sesegera mungkin melalui perekaman dan interpretasi EKG 12 sadapan, selambatlambatnya 10 menit dari saat pasien tiba untuk mendukung penatalaksanaan yang berhasil. • Semua rumah sakit dan Sistem Emergensi Medis yang terlibat dalam penanganan pasien STEMI harus mencatat dan mengawasi segala penundaan yang terjadi dan berusaha utk mencapai & mempertahankan target kualitas berikut ini: 1. Waktu dari kontak medis pertama hingga perekaman EKG pertama ≤10 menit 2. Waktu dari kontak medis pertama hingga pemberian terapi reperfusi: • Untuk fibrinolisis ≤30 menit • Untuk IKP primer ≤90 menit (≤60 menit apabila pasien datang dengan awitan kurang dari 120 menit atau langsung dibawa ke rumah sakit yang mampu melakukan IKP)

• Terapi reperfusi (sebisa mungkin berupa IKP primer) diindikasikan apabila terdapat bukti klinis maupun EKG adanya iskemia yang sedang berlangsung, bahkan bila gejala > 12 jam yang lalu atau jika nyeri dan perubahan EKG tampak tersendat. • Dalam menentukan terapi reperfusi, tahap pertama adalah menentukan ada tidaknya rumah sakit sekitar yang memiliki fasilitas IKP. • Bila tidak ada, langsung pilih terapi fibrinolitik. • Bila ada, pastikan waktu tempuh dari tempat kejadian (baik rumah sakit atau klinik) ke rumah sakit tersebut apakah kurang atau lebih dari (2 jam).

• Jika membutuhkan waktu lebih dari 2 jam, reperfusi pilihan adalah fibrinolitik. Setelah fibrinolitik selesai diberikan, jika memungkinkan pasien dapat dikirim ke pusat dengan fasilitas IKP.

http://www.inaheart.org/upload/file/Pedoman_tatalaksana_Sindrom_Koroner_Akut_2015.pdf

Ventrikular takikardi

Monomorphic Ventrikular takikardi • Patofisiologi

• Manifestasi klinis

- Konduksi impuls diperlambat di sekitar area cedera ventrikel, infark, atau iskemia.

- Gejala dari penurunan cardiac output (ortostasis, hipotensi, sinkop, menurunnya aktivitas fisik).

- Area ini juga berfungsi sebagai sumber impuls ektopik (fokus iritasi).

- Dapat asimtomatik.

- Area cedera ini dapat menyebabkan dorongan untuk mengambil jalan melingkar, yang mengarah ke reentry phenomenon dan depolarisasi berulang cepat.

- VT yang tidak diobati dan berkelanjutan dapat memburuk menjadi unstable VT dan VF.

• EKG - Rate : ventricular rate >100 bpm (biasanya 120-250 bpm). - Rhythm : regular ventricular rhythm. - PR : absent (AV dissociated). - P waves : jarang terlihat namun ada. - QRS complex : melebar dan ganjil, “PVC-like” complexes ≥0,12 s, dengan T waves yang besar polaritas berlawanan dari QRS.

ACLS 2016

Polimorphic Ventrikular takikardi • Patofisiologi

• Manifestasi klinis

- Konduksi impuls diperlambat di beberapa area cedera ventrikel, infark, atau iskemia.

- Biasanya akan cepat memburuk menjadi pulseless VT atau VF.

- Area ini juga berfungsi sebagai sumber impuls ektopik (fokus iritasi), terjadi di beberapa area ventrikel sehingga disebut polimorfik.

- Gejala penurunan cardiac output (ortostasis, hipotensi, perfusi yang buruk, sinkop) terjadi sebelum pulseless arrest.

- Area cedera ini dapat menyebabkan dorongan untuk mengambil jalan melingkar, yang mengarah ke reentry phenomenon dan depolarisasi berulang cepat. • EKG - Rate : ventricular rate >100 bpm (biasanya 120-250 bpm). - Rhythm : regular atau irregular ventricular, tidak ada aktivitas atrial.

- PR : tidak ada. - P waves : jarang namun ada, VT merupakan bentuk AV dissociation. - QRS complexes : variasi dan inkonsistensi yang tampak.

ACLS 2016

Torsades de pointes • Patofisiologi - QT interval memanjang dan menyebabkan peningkatan periode refraktori relatif (vulnerable period) dari siklus jantung. Peningkatan ini memungkinkan fokus iritasi terjadi pada T wave (vulnerable period or R on T phenomenon). - R on T phenomenon sering menimbulkan VT.

• Manifestasi klinis - Kecenderungan menuju perburukan mendadak ke VT pulseless atau VF. - Gejala penurunan cardiac output.

- Stable torsades, torsade berkelanjutan jarang terlihat.

• EKG

- Atrial rate : tidak dapat ditentukan. - Ventricular rate : 150-250 bpm. - Rhythm : irregular ventricular rhythm. - PR : tidak ada. - QRS complexes : spindle node pattern.

ACLS 2016

Supraventrikular takikardi

Supraventrikular takikardi :Gangguan irama jantung • Gejala: Heart rate: >150 detak/menit • • • • • • •

Sesak nafas(S) Terasa palpitasi di dada (S) Pusing (S) Nafas cepat (S) Mati rasa pad beberapa bagian tubuh (S) Nyeri dada terus menerus (U) Penurunan kesadaran (U)

• Diagnosis: gejala & EKG

• Tatalaksana: Pertimbangkan yang mana yang harus diberikan • • • •

Vagal Maneuvers Medications Support Airway, Breathing, Circulation Unstable → synchronized cardioversion (50-100J)

Manuver vagal • Bearing down disebut juga sebagai manuver Valsava → Pasien diinstruksikan untuk menahan seolah-olah mereka sedang buang air besar/meniup sedotan yang tersumbat selama beberapa detik → meningkatkan tekanan intratoraks dan menstimulasi saraf vagus. • Carotid Massage Pemijatan leher pasien dengan memberikan tekanan yang diterapkan dengan gerakan sirkuler yang lembut di bawah rahang selama 10 detik • Batuk Batuk kuat dan terus menerus → meningkatkan tekanan intratoraks dan menstimulasi saraf vagus. • Muntah Memasukkan depressor lidah ke bagian belakang tenggorokan → refleks muntah. → merangsang saraf vagus. • Cold Stimulus to the Face menenggelamkan wajah dalam air es → vasokontriksi sistemik → bradikardia

Ventricular fibrilasi

Ventrikular fibrilasi • Disordered electrical activity causes the heart’s lower chambers (ventricles) to quiver, or fibrillate, instead of contracting (or beating) normally. This prohibits the heart from pumping blood, causing collapse and cardiac arrest. • The ECG shows a fine-to-coarse zigzag pattern without discernible P waves or QRS complexes. • VF is seen most commonly in patients with severe ischemic heart disease, with or without an acute MI. It also can be caused by digoxin or quinidine toxicity, hypothermia, chest trauma, hypokalemia, hyperkalemia, or mechanical stimulation • Primary VF occurs suddenly, without preceding hemodynamic deterioration, and usually is due to acute ischemia or peri-infarct scar reentry. • Secondary VF occurs after a prolonged period of hemodynamic deterioration due to left ventricular failure or circulatory shock. http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/Ventricular-Fibrillation_UCM_324063_Article.jsp Tintinalli’s emergency medicine manual. 7th Edition. USA: McGraw-Hill Education, 2017.

• Etiologi • Insufficient blood flow to the heart muscle • Damage to the heart muscle (from a heart attack, for example) • Cardiomyopathy • Problems with the aorta • Drug toxicity • Sepsis (severe body infection)

Ventrikular fibrilasi: diagnosis dan tatalaksana • suddenly collapse or become unconscious • The following symptoms may occur within minutes to 1 hour before the collapse: • Chest pain • Dizziness • Nausea • Rapid heartbeat • Shortness of breath • Sign of cardiac arrest: • Sudden loss of responsiveness (no response to tapping on shoulders) • No normal breathing (the victim is not breathing or is only gasping) • This is sudden cardiac arrest (SCA) -- which requires immediate medical help (CPR and defibrillation)

Tatalaksana 1.

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3.

4.

Perform immediate electrical defibrillation (unsynchronized) at 200 J (biphasic) and 360 J (monophasic) along with immediate vigorous chest compressions to augment coronary perfusion. Keep defibrillation pads on the patient and in the same location because, with successive countershocks, transthoracic impedance decreases. If the initial two cycles of cardiopulmonary resuscitation (CPR) and defibrillation are unsuccessful, administer antiarrhythmic treatment using amiodarone 300 mg IV push. Lidocaine is second-line and is dosed at 1.5 mg/kg IV followed by 0.75 mg/kg IV for two more doses. Repeat the CPR-defibrillation cycle. If no pulse is present after the third CPR-defibrillation cycle, give epinephrine 1 mg IV push, or vasopressin 40 units IV push (one time only), followed by a 20-mL normal saline flush and immediate resumption of the CPRdefibrillation cycle. In refractory VF, administer magnesium sulfate 1 to 2 g IV over 60 to 90 seconds followed by an infusion of 1 to 2 g/h. http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/VentricularFibrillation_UCM_324063_Article.jsp Tintinalli’s emergency medicine manual. 7th Edition. USA: McGraw-Hill Education, 2017.

Cardiorespiratory arrest

Cardiorespiratory arrest • Henti jantung adalah terhentinya fungsi pompa jantung secara tiba-tiba, yang dapat reversible tetapi akan mengakibatkan kematian jika tidak dilakukan penangananan segera. • Henti jantung dapat disebabkan o/ 4 gangguan irama jantung: fibrilasi ventrikel, takikardi ventrikel tanpa nadi, pulseless electric activity (PEA), dan asistol. • Tatalaksana awal: resusitasi jantung paru (RJP) dan defibrilasi dalam menit awal henti jantung (u/ irama VF dan VT tanpa nadi) EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar

Harrison’s principal of internal medicine

Pulseless ventricular tachycardia : takikardi dengan kompleks QRS yg lebar yg berasal dari ventrikel, disebabkan oleh reentry, triggered activity, atau automaticity. • Diagnosis: • Penurunan kesadaran tiba-tiba • Terdapat henti napas • Tidak ada denyut nadi

• Pemeriksaan EKG • • • • • •

Disosiasi atrioventricular Kompleks QRS yg lebar (>0,16 detik) Perubahan aksis Kompleks QRS 90-180x/mnt Capture beat & fusion beat Morfologi: monomorfik / polimorfik

• Tatalaksana: Defibrilasi sesegera mngkin, diikuti RJP, pemberian obat-obatan, dan tatalaksana penyebab • Defibrilasi nonsynchronized mnggunaakn energi 360 J dg gelombang monofasik dan 120-200 J dg gelombang bifasik • RJP 5 siklus dilakukan jika ps belum dipasang ETT. Jika ps telah dipasang, berikan ventilasi 8-10 x/mnt + kompresi dada 100x/mnt • Perlu dicari factor penyebab yg dapat dikoreksi spt iskemia, gg elektrolit, hipotensi, dan asidosis

EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.

Asistol : suatu keadaaan dimana tidak tdpt aktivitas • Pemeriksaan EKG: listrik dan aktivitas mekanik dari jantung (tidak • Tdk terlihat adanya aktivitas ventrikel atau ≤6 kompleks/menit tdpt frakuensi ventrikel atau iramanya, tidak • R tdk dapat ditetapkan & terkadang terlihat gel. P ada denyut, dan tidak ada curah jantung) • Etiologi: • Primer: hypovolemia, hipoksia, hipotermia, hipo/hiperkalemia, dan asidosis • Sekunder: tamponade jantung, tension pneumothoraks, thrombosis paru (emboli paru massif), thrombosis jantung (sindrom coroner akut), toksin akibat overdosis obat.

• Diagnosis: • Penurunan kesadaran tiba-tiba • Terdapat henti napas • Tidak ada denyut nadi

• Gel. R tdk tampak • Kompleks QRS tdk terlihat adanya defleksi yg konsisten dg suatu kompleks QRS

• Tatalaksana: • RJP segera sebanyak 5 siklus, sambal pertimbangkan pemberian obat-obatan berupa epinefrin dan vasopressin  stelah 5 siklus, cek irama jantung dan tatalaksana sesuai algoritme • Pemberian obat-obatan: • Epinefin: 1 mg IV (diulang setiap 3-5 mnt) selama henti jantung. Pemberian IV bolus dg bantuan 20 mL cairan iv + peninggian ekstremitas 10-20 dtk  jika tdk ada jalur IV, dapat mll jalur ETT dosis 2-2,5 mg dilarutkan dalam 5-10 mL cairan fisiologis • Vasopresin: dosis tunggal 400 U IV menggantikan dosis pertama atau kedua epinefrin. EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.

Aktivitas listrik tanpa denyut (PEA) • Hiperkalemia (penginkatan gel. P, blok jantung : suatu keadaaan dimana masih terdapat yg komplit, centricular escape rhythm) aktivitas listrik jantung tanpa disertai respon • Infark miokard akut mekanik jantung berkontraksi untuk • Overdosis obat spt antidepresan trisiklik: menghasilkan denyut yg teraba atau pemanjangan durasi kompleks QRS tekanan darah yang terukur. • Tatalaksana: • Etiologi: • Primer: hypovolemia, hipoksia, hipotermia, hipo/hiperkalemia, dan asidosis • Sekunder: tamponade jantung, tension pneumothoraks, thrombosis paru (emboli paru massif), thrombosis jantung (sindrom coroner akut), toksin akibat overdosis obat.

• Diagnosis: • Pasien tidak sadar • Tidak bernapas • Tidak ditemukan denyut nadi

• Pemeriksaan EKG: menunjukkan fx penyebab

• RJP segera sebanyak 5 siklus, sambal pertimbangkan pemberian obat-obatan berupa epinefrin dan vasopressin  stelah 5 siklus, cek irama jantung dan tatalaksana sesuai algoritme • Pemberian obat-obatan:

• Epinefin: 1 mg IV (diulang setiap 3-5 mnt) selama henti jantung. Pemberian IV bolus dg bantuan 20 mL cairan iv + peninggian ekstremitas 10-20 dtk  jika tdk ada jalur IV, dapat mll jalur ETT dosis 2-2,5 mg dilarutkan dalam 5-10 mL cairan fisiologis • Vasopresin: dosis tunggal 400 U IV menggantikan dosis pertama atau kedua epinefrin. EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.

Gagal jantung akut

Gagal jantung adalah sindrom klinis yang ditandai dengan gejala khas (misalnya sesak napas, pergelangan kaki bengkak dan kelelahan) yang bisa disertai dengan tanda-tanda (misalnya peningkatan tekanan vena jugularis, crackles paru dan edema perifer) yang disebabkan oleh kelainan jantung struktural dan / atau fungsional, sehingga sebuah penurunan curah jantung dan / atau tekanan intrakardiak tinggi pada saat istirahat atau selama stres.

Rosen’s Emergency Medicine, 9th ed.

European Heart Journal. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.2012:33;1842-32

Gagal jantung akut: definisi dan etiologi

Gagal jantung akut: Tanda dan gejala • Cardinal symptoms  fatigue and shortness of breath • In the early stages of HF, dyspnea is observed only during exertion; however, as the disease progresses, dyspnea occurs with less strenuous activity, and it ultimately may occur even at rest

• Cheyne-stokes respiration  caused by a diminished sensitivity of the respiratory center to arterial Pco2 • Acute pulmonary edema • Gastrointestinal symptoms

• Orthopnea  dyspnea occurring in the recumbent position, is usually a later manifestation of HF than is exertional dyspnea • Nocturnal cough • Paroxysmal nocturnal dyspnea (PND)  refers to acute episodes of severe shortness of breath and coughing that generally occur at night and awaken the patient from sleep, usually 1–3 h after the patient retires Sumber: Harrison’s Cardiovascular Medicine, 2th ed.

Gagal jantung akut: Pemeriksaan Pemeriksaan fisik

Pemeriksaan lain

• General appearance and vital signs  patient appears to be in no distress at rest except for feeling uncomfortable when lying flat for more than a few minutes, systolic blood pressure may be normal or high in early HF, but it generally is reduced in advanced HF because of severe LV dysfunction, the pulse pressure may be diminished, reflecting a reduction in stroke volume, sinus tachycardia, cool peripheral extremities and cyanosis of the lips and nail bed

• Routine laboratory testing

• Jugular veins  In the early stages of HF, the venous pressure may be normal at rest but may become abnormally elevated with sustained (∼1 min) pressure on the abdomen (positive abdominojugular reflux).

• Exercise testing

• Electrocardiogram (ECG) • CXR • Assessment of LV function

• Biomarkers

• Pulmonary examination  pulmonary crackles (rales or crepitations) • Cardiac examination  If cardiomegaly is present, the point of maximal impulse (PMI) usually is displaced below the ffth intercostal space and/or lateral to the midclavicular line, and the impulse is palpable over two interspaces.

• Abdomen and extremities • Cardiac cachexia

Sumber: Harrison’s Cardiovascular Medicine, 2th ed.

European Heart Journal. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.2012:33;1842-32

Algoritma Diagnosis

Algoritma tatalaksana

Rosen’s Emergency Medicine,

9th

ed.

European Heart Journal. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.2012:33;1842-32

Gagal jantung akut: Tatalaksana Farmakologi

European Heart Journal. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.2012:33;1842-32

Diseksi aorta

Diseksi aorta : pemisahan lapisan tunika media oleh darah, yg meluas secara progresif ke proksimal atau distal dari aorta. Lapisan dalam dari dinding aorta mengalami robekan, sdgkn lapisan luar utuh  darah mengalir mll robekan dan membelah lapisan tengah dinding aorta dan membentuk saluran baru di dalam dinding aorta.

• Gambaran klinis:

• Sakit dada atau punggung dg rasa sakit spt tertusuk benda tajam • Rasa sakit yg timbul tiba-tiba • Denyut yg lemah atau tidak ada denyut pd brakialis (pulse deficit) • Hipertensi • Rasa sakit berpindah-pindah

• Diagnosis: gejala klinis + adanya pelebaran aorta atau mediastinal pada pemeriksaan radiografi • Diagnosis banding: • • • • • •

Iskemia miokard Perikarditis Emboli paru Nyeri otot Pleuritis Kolesistitis

• Aterosklerotik • Tumor mediastinal • Pankreatitis akut

• Pemeriksaan:

• Lab: peningkatan CRP, leukositosis ringan hingga sedang, dan sedikit peningkatan LDH • Pd ps yg tiba dg onset <24 jam, kadar D-dimer <500ng/mL • EKG: hipertrofi ventrikel kiri akibat hipertensi yg lama • Foto thoraks: pelebaran mediastinum superior, bayangan ganda dinding aorta, dan perbedaan ukuran aorta asenden dan desenden. Kadang adijumpai kardiomegali sekunder karena efusi pericardial atau tanda efusi pleura. • Retrograde aortography • CT-scan • MRI: sensitivitas 85%, spesifisitas 100% • Echocardiography • Transthoracic echocardiographt (TTE): sensitivitas 60-80% dan spesifitas 83-96% • Transesophageal echocardiography (TEE): spesifisitas 8295% & sensitivitas 92-100% • Intraoperatif epicardial ekokardiografi enamel epitel (IEE) • Intravascular ultrasound (iVUS)

EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.

Diseksi aorta • Obat yang digunakan untuk terapi medis: • Pasien dgn dugaan diseksi aorta akut • Natrium Nitroprusside harus dirawat intensif untuk evaluasi diagnostic segera. • Nitrogliserin • Nikardipin • Morfin sulfat  menghilangkan nyeri • Clevidipine • Beta blocker iv (metoprolol, propranolol, • Fenoldopam labetalol)  mengontrol target tek darah • Beta Blocker sistolik 110 mmHg • Tindakan bedah: • Pilihan terapi bedah  untuk Stanford • Indikasi : semua pasien dengan diseksi tipe A (aorta asendens) proksimal dgn pengecualian pasien kondisi serius yg menghalangi operasi • Pilihan terapi medis  untuk Stanford tipe B (aorta desenden tmsk diseksi aorta • Teknik yg sering digunakan utk diseksi aorta asenden : Bentall, cabrol, button, elephant abdominal) trunk • Terapi medis: • Terapi intervensi pemasangan stent: Hasil • Pengobatan antihipertensi secara iv harus dari pemasangan stent menyebabkan segera dimulai pada semua pasien diseksi perbaikan aliran darah pd pembuluh darah aorta akut kecuali ps hipotensi. yg tersumbat akibat diseksi aorta • Th/ standard saat ini: kombinasi dari beta blocker dan vasodilator (natrium nitroprusside)

EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.

Diseksi aorta • Komplikasi: dapat menyebabkan oklusi cabang aorta  kerusakan pada organ • Murmur diastolic aorta (50% kasus) karena regurgitasi aorta • Gagal jantung • Tamponade jantung • Gejala neurologis dapat ditemukan • Pd keterlibatan A. celiac: nyeri perut terums-menerus, meningktnya protein fase akut, dan peningkatan laktat dehydrogenase.

rasa sakit yg hebat, timbulnya syok, deficit pulse, dan adanya deifisit neurologis • Tingkat kelangsungan hidup jangka pjg ps diseksi aorta proksimal yg menjalani tindakan bedah: 65-80% pd 5 tahun dan 40-50% pd 10 tahun • Penyebab plg umum kematian jangka panjang dari diseksi aorta adl pecahnya aorta dan mengakibatkan diseksi berikutnya atau aneurisma.

• Prognosis: • Angkat kematian ps diseksi aorta proksimal: 30% dan pd diseksi aorta distal 10% • Mortalitas meningkat pd ps usia 65 th,

EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.

Kesimpulan kasus pemicu • Pasien datang dengan keluhan nyeri dada 3 jam yang lalu disertai mual muntah dan banyak berkeringat. Setelah dilakukan pemeriksaan EKG, didapatkan hasil infark miokard. Setelah beberapa saat kemudian, pasien mengalami ventrikel fibrilasi dengan gejala kejang dan kehilangan kesadaran

Daftar Pustaka • EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar. Editor: Setyohadi B, Arsana PM, Soeroto AY, Suryanto A, Abdullah M. 2015. Jakarta: Interna Publishing • Buku Ajar Ilmu Penyakit Dalam Ed VI • Harrison’s principal of internal medicine • Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011. • Rosen’s Emergency Medicine, 9th ed • Dharma, S. Cara Mudah Membaca EKG. Jakarta: EGC; 2017. • European Heart Journal. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.2012:33;1842-32 • GW Reed et al. The Lancet; 2017 • https://www.uscjournal.com/articles/st-segment-elevation-myocardial-infarction-challenges-diagnosis • Toronto. Essential med notes 2015. • ACLS 2016 • Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health • Zipes DP, Libby P, Bonow RO, Mann DL, Braunwald E. Braunwald’s heart disease: a textbook of cardiovascular medicine, 11th Edition. Philadelphia: Elsevier Inc.; 2019. • ESC Guidelines for the management of ACS in patients presenting without persistent ST-segment elevation. The European Society of Cardiology, 2015 • AHA/ACC Guideline for the management of patients with non ST-elevation acute coronary syndromes; 2014 • http://www.inaheart.org/upload/file/Pedoman_tatalaksana_Sindrom_Koroner_Akut_2015.pdf