6thProblem

Emergency Medicine Block

Group 10
October 29th, 2018
Group member
Tutor: dr. Agus
Ketua : Kurnia Elsa Oktaviana 405150111
Sekretaris : Erika Juniartha Tungki 405150002
Penulis : Marshally Safira Masrie 405150104
Anggota:
• Maria Meilani Christina 405140127
• Elfinder Singh Dhillon 405140180
• Stevanno Geraldus 405150037
• Merlyn Priscilla 405150044
• Timmy Yonatan Nangoy 405150100
• Clareta Vero Patricia W 405150132
• Irwan Surya Angkasa 405150170
• Thalia Christabel 405150196
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 Acute Coronary

Cardiorespiratory arrest
arrest Syndrome

Diseksi aorta

Acute cor Acute cardiac Angina Miokard

Aritmia
pulmonale failure pectoris infark

Supraventrikular Ventrikular Ventrikel Unstable angina

STEMI NSTEMI
takikardi takikardi fibrilasi pectoris
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
Thrombosis arteri
ATEROSKLEROTIK
ETIOLOGI koroner
Coronary emboli from
mechanical or infected cardiac
valves

Inflammation from acute

vasculitis
NON -
ATEROSKLEROTIK
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. Angina pectoris 6. Ventrikular fibrilasi
2. Acute cor pulmonal 7. Cardiorespiratory arrest
3. Miokard infark 8. Acute cardiac failure
4. Ventrikular takikardi 9. Diseksi aorta
5. Supraventrikular takikardi
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) • Etiologi: • Obesity
or dilation caused by elevated • Chronic hypoxia • Pulmonary veno-occlusive
pulmonary artery pressure. • COPD disease
• RVH due to a systemic defect or • High-altitude dwellers • Pulmonary vascular
congenital heart disease is not • Sleep apnea obstruction secondary to
classified as cor pulmonale. • Chest deformities tumors or adenopathy
• Acute cor pulmonale: • Kyphoscoliosis • Increased blood viscosity:
• Right ventricle is dilated & muscle wall • Pulmonary embolism • Polycythemia vera
stretched thin • Interstitial lung disease • Leukemia
• Overload due to acute pulmonary • Scleroderma • Increased intrathoracic
hypertension (HTN) • Systemic lupus erythematosus pressure:
• Most often caused by massive • Mixed connective tissue • Mechanical ventilation with
pulmonary embolism disease positive end-expiratory
• pressure
• Chronic cor pulmonale: Sarcoidosis
• Pulmonary Langerhans cell • Idiopathic primary pulmonary
• RVH with eventual dilation and right-
sided heart failure histiocytosis HTN
• Caused by an adaptive response to • Neurofibromatosis
chronic pulmonary HTN • Lymphangioleiomyomatosis
• Predominately occurs as a result of • Cystic fibrosis
alveolar hypoxia • Severe anemia

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health
Acute cor pulmonale: manifestasi klinis
• Tanda dan gejala: End-stage cor pulmonale • Physical-Exam
• Exertional dyspnea • Cardiogenic shock • Jugular venous distention
• Easy fatigability •
• Oliguria Prominent A- and V-waves
• Weakness
• Cool extremities • Increase in chest diameter
• Exertional syncope
• Pulmonary edema secondary to • Crackles and/or wheezes
• Cough
• Hemoptysis intraventricular septum impairing • Left parasternal heave on
left ventricular diastolic function cardiac palpation
• Exertional angina even in the
absence of coronary disease • Splitting of the 2nd heart
sound or murmurs of the
• Anorexia • Riwayat: pulmonary vasculature may
• Right upper quadrant • Exercise intolerance
discomfort be heard.
• Palpitations • Hepatojugular reflex and
• Wheezing
• Chest pain pulsatile liver
• Hoarseness
• Lightheadedness • Pitting edema of the lower
• Weight gain
• Syncope extremities
• Hepatomegaly
• Swelling of the lower
• Ascites extremities
• Peripheral edema

Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health
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.
Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH EDITION 2015 by Wolters Kluwer Health
1. CXR: Signs of pulmonary HTN: 3. MRI
• Large pulmonary arteries (>16–18 • Superior to echocardiography for
mm) assessment of right ventricular
• An enlarged RV silhouette size & function
• Pleural effusions do not occur in the
4. Pulmonary function tests
setting of cor pulmonale alone.
• Impaired diffusion capacity due to
2. Echocardiography pulmonary HTN
• The noninvasive diagnostic method 5. Right-heart catheterization:
of choice
• The most precise estimate of
• RV dilation or RVH pulmonary vascular
• Assessment of tricuspid hemodynamics
regurgitation • Gives accurate measurements of
pulmonary arterial pressure and
3. Chest CT, ventilation/ pulmonary capillary wedge
perfusion scans, or pulmonary pressure
angiography:
• Useful in the setting of acute cor
pulmonale
Acute cor pulmonale: Pemeriksaan & DD
6. EKG: • Small R-waves and deep S-waves across DIFFERENTIAL DIAGNOSIS
the precordium
• Right-axis deviation • Primary disease of the left
• Right atrial enlargement; Tall, peaked
• Right bundle branch block P-waves (P pulmonale) 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 • Congenital heart disease
• Prominent S-wave in V5 and V6 • 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/abnormal- Rosen & Barkin’s 5-Minute Emergency Medicine Consult 5TH

ecg?pa=8nN9RPXta4tZ9RtmOofVGdBR4rzs%2FEqqnJ5hIz8dvPJ0JqBZYWZu%2Bl2yQYktlC1GJyGvMX%2Fu%2BWdIXoARf%2FT0zw%3D%3D
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 • Improving oxygenation reduces pulmonary arterial
vasoconstriction and RV afterload.
• IV access • The improved cardiac output enhances diuresis of
• Cardiac monitoring excess body water.

• Pulse oximetry • Care must be taken to monitor the patient’s ventilatory

status and PCO2, as hypercapnia may reduce
• Treat bronchospasm from associated respiratory respiratory drive and cause acidosis.
disease:
• Diuretics: furosemide  added cautiously to reduce
• β-Agonist nebulizers pulmonary artery pressure by contributing to the
reduction of circulating blood volume:
• Be wary of volume depletion and hypokalemia
INITIAL STABILIZATION/THERAPY
• Patients should be maintained on salt and fluid
• ED therapy is directed at the underlying disease restriction.
process and reducing pulmonary HTN. • 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 • Furosemide: 20–60 mg IV
those patients with COPD • (peds: 1 mg/kg may increase by 1 mg/kg/q2h not to
• Selective β-adrenergic agents: terbutaline 0.25 mg exceed 6 mg/kg)
SC may be useful. • Terbutaline: 0.25 mg SC
• Bronchodilator affects and reduces ventricular DISPOSITION
afterload. • Admission Criteria
• Theophylline may play a role to improve • New-onset hypoxia
diaphragmatic contractility & << muscle fatigue. • Anasarca: extreme generalized edema
• Anticoagulation may be considered for those at • Severe respiratory failure
high risk for • Admission criteria for the underlying disease process
• thromboembolic disease. • Discharge Criteria
• Acutely decompensated COPD patients: • Patients without hypoxia or a stable oxygen
• Early steroid therapy requirement
• Antibiotic administration • Issues for Referral
• Close follow-up as long as the underlying etiology has
responded to acute management
In general, improvement in the underlying • The need for a sleep study to assess for sleep apnea
respiratory disease results in improved RV function. 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, ESC Guidelines for the management of acute coronary syndromes in patients presenting without
persistent ST-segment elevation. The European Society of Cardiology, 2015
isolated dyspnoe (umum pada orang
tua, wanita dan pasien DM, penyakit
ginjal kronik, demensia)

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 • In most cases, the diagnosis of STEMI can be made
the chest, often radiating to the neck, jaw, shoulder, or arm. quickly once the person is under medical care.
Profuse sweating, breathlessness, and a profound sense of A review of symptoms, accompanied by the
impending doom also common. At times, the signs may be far less evaluation of the ST segment on the ECG, is usually
obvious, manifesting with nonspecific or generalized enough for a doctor to begin treatment.
symptoms such as: • A review of cardiac enzymes may also help but usually
• Pain around the shoulder blades, arm, chest, jaw, left arm, or arrives well after acute treatment is started.
upper abdomen
• It is important to stabilize the person as quickly as
• A painful sensation described as having a "clenched fist in the
chest" possible.
• Discomfort or tightness in the neck or arm • In addition to pain and distress, STEMI can cause
sudden death due to ventricular fibrillation (a serious
• Indigestion or heartburn disturbance of the heart rhythm) or acute heart failure
• Nausea and vomiting (when the heart cannot pump enough blood to
properly supply the body).
• Fatigue or sudden exhaustion
• Shortness of breath • After a heart attack has run its course, the muscle
• Dizziness or lightheadedness
itself may be left with substantial permanent damage.
• Increased or irregular heart rate • Chronic heart failure is a common consequence of
• Clammy skin
this, as is the increased risk of dangerous cardiac
arrhythmias (irregular heartbeats ).
https://www.verywellhealth.com/stemi-st-segment-elevation-myocardial-infarction-1746032
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 • Terapi reperfusi segera, baik dengan IKP atau farmakologis, diindikasikan
berdasarkan riwayat nyeri dada yang berlangsung selama 20 untuk semua pasien dengan gejala yang timbul dalam 12 jam dengan
menit atau lebih yang tidak membaik dengan pemberian
nitrogliserin. 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, selambat- • Terapi reperfusi (sebisa mungkin berupa IKP primer) diindikasikan apabila
lambatnya 10 menit dari saat pasien tiba untuk mendukung
penatalaksanaan yang berhasil. terdapat bukti klinis maupun EKG adanya iskemia yang sedang
berlangsung, bahkan bila gejala > 12 jam yang lalu atau jika nyeri dan
• Semua rumah sakit dan Sistem Emergensi Medis yang
terlibat dalam penanganan pasien STEMI harus mencatat perubahan EKG tampak tersendat.
dan mengawasi segala penundaan yang terjadi dan berusaha
utk mencapai & mempertahankan target kualitas berikut ini: • Dalam menentukan terapi reperfusi, tahap pertama adalah menentukan
1. Waktu dari kontak medis pertama hingga perekaman EKG ada tidaknya rumah sakit sekitar yang memiliki fasilitas IKP.
pertama ≤10 menit
• Bila tidak ada, langsung pilih terapi fibrinolitik.
2. Waktu dari kontak medis pertama hingga pemberian terapi
reperfusi: • Bila ada, pastikan waktu tempuh dari tempat kejadian (baik rumah sakit
atau klinik) ke rumah sakit tersebut apakah kurang atau lebih dari (2 jam).
• Untuk fibrinolisis ≤30 menit
• Untuk IKP primer ≤90 menit (≤60 menit apabila pasien • Jika membutuhkan waktu lebih dari 2 jam, reperfusi pilihan adalah
datang dengan awitan kurang dari 120 menit atau langsung fibrinolitik. Setelah fibrinolitik selesai diberikan, jika memungkinkan pasien
dibawa ke rumah sakit yang mampu melakukan IKP)
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
- Konduksi impuls diperlambat di sekitar area cedera
ventrikel, infark, atau iskemia.
- Area ini juga berfungsi sebagai sumber impuls ektopik
(fokus iritasi).
- Area cedera ini dapat menyebabkan dorongan untuk
mengambil jalan melingkar, yang mengarah ke reentry
phenomenon dan depolarisasi berulang cepat.
• Manifestasi klinis
- Gejala dari penurunan cardiac output (ortostasis,
hipotensi, sinkop, menurunnya aktivitas fisik).
- Dapat asimtomatik.
- 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 - Biasanya akan cepat memburuk menjadi pulseless VT
ventrikel, infark, atau iskemia. atau VF.
- Area ini juga berfungsi sebagai sumber impuls ektopik - Gejala penurunan cardiac output (ortostasis, hipotensi,
(fokus iritasi), terjadi di beberapa area ventrikel perfusi yang buruk, sinkop) terjadi sebelum pulseless
sehingga disebut polimorfik. 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 • Manifestasi klinis
- QT interval memanjang dan menyebabkan - Kecenderungan menuju perburukan mendadak ke VT
peningkatan periode refraktori relatif (vulnerable pulseless atau VF.
period) dari siklus jantung. Peningkatan ini
- Gejala penurunan cardiac output.
memungkinkan fokus iritasi terjadi pada T wave
(vulnerable period or R on T phenomenon). - Stable torsades, torsade berkelanjutan jarang
terlihat.
- R on T phenomenon sering menimbulkan VT.

• 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 • Tatalaksana: Pertimbangkan yang mana yang
• Gejala: Heart rate: >150 detak/menit harus diberikan
• Sesak nafas(S) • Vagal Maneuvers
• Medications
• Terasa palpitasi di dada (S)
• Support Airway, Breathing, Circulation
• Pusing (S)
• Unstable → synchronized cardioversion (50-100J)
• Nafas cepat (S)
• Mati rasa pad beberapa bagian tubuh (S)
• Nyeri dada terus menerus (U)
• Penurunan kesadaran (U)
• Diagnosis: gejala & EKG
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 • Etiologi
chambers (ventricles) to quiver, or fibrillate, instead of • Insufficient blood flow to the heart
contracting (or beating) normally. This prohibits the heart muscle
from pumping blood, causing collapse and cardiac arrest. • Damage to the heart muscle (from a
• The ECG shows a fine-to-coarse zigzag pattern without heart attack, for example)
discernible P waves or QRS complexes. • Cardiomyopathy
• Problems with the aorta
• VF is seen most commonly in patients with severe
ischemic heart disease, with or without an acute MI. It • Drug toxicity
also can be caused by digoxin or quinidine toxicity, • Sepsis (severe body infection)
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.
Ventrikular fibrilasi: diagnosis dan tatalaksana
• suddenly collapse or become unconscious Tatalaksana
• The following symptoms may occur within minutes to 1 hour 1. Perform immediate electrical defibrillation
before the collapse: (unsynchronized) at 200 J (biphasic) and 360 J
• Chest pain (monophasic) along with immediate vigorous chest
• Dizziness compressions to augment coronary perfusion. Keep
• Nausea defibrillation pads on the patient and in the same location
• Rapid heartbeat because, with successive countershocks, transthoracic
• Shortness of breath impedance decreases.
• Sign of cardiac arrest: 2. If the initial two cycles of cardiopulmonary resuscitation
• Sudden loss of responsiveness (no response to tapping on (CPR) and defibrillation are unsuccessful, administer
shoulders) antiarrhythmic treatment using amiodarone 300 mg IV
• No normal breathing (the victim is not breathing or is only push. Lidocaine is second-line and is dosed at 1.5 mg/kg IV
gasping) followed by 0.75 mg/kg IV for two more doses. Repeat the
• This is sudden cardiac arrest (SCA) -- which requires CPR-defibrillation cycle.
immediate medical help (CPR and defibrillation) 3. 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 CPR-
defibrillation cycle.
4. 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/Ventricular-
Fibrillation_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.

• Tatalaksana: Defibrilasi sesegera mngkin,

• Diagnosis:
diikuti RJP, pemberian obat-obatan, dan
• Penurunan kesadaran tiba-tiba
tatalaksana penyebab
• Terdapat henti napas
• Defibrilasi nonsynchronized mnggunaakn energi
• Tidak ada denyut nadi 360 J dg gelombang monofasik dan 120-200 J dg
gelombang bifasik
• Pemeriksaan EKG • RJP 5 siklus dilakukan jika ps belum dipasang ETT.
Jika ps telah dipasang, berikan ventilasi 8-10 x/mnt
• Disosiasi atrioventricular
+ kompresi dada 100x/mnt
• Kompleks QRS yg lebar (>0,16 detik)
• Perlu dicari factor penyebab yg dapat dikoreksi spt
• Perubahan aksis iskemia, gg elektrolit, hipotensi, dan asidosis
• Kompleks QRS 90-180x/mnt
• Capture beat & fusion beat
• Morfologi: monomorfik / polimorfik
EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.
Asistol
: suatu keadaaan dimana tidak tdpt aktivitas
listrik dan aktivitas mekanik dari jantung (tidak
tdpt frakuensi ventrikel atau iramanya, tidak
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
• Pemeriksaan EKG:
• Tdk terlihat adanya aktivitas ventrikel atau ≤6
kompleks/menit
• R tdk dapat ditetapkan & terkadang terlihat gel. P
• 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)
: suatu keadaaan dimana masih terdapat
aktivitas listrik jantung tanpa disertai respon
mekanik jantung berkontraksi untuk
menghasilkan denyut yg teraba atau
tekanan darah yang terukur.
• 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
• Hiperkalemia (penginkatan gel. P, blok jantung
yg komplit, centricular escape rhythm)
• Infark miokard akut
• Overdosis obat spt antidepresan trisiklik:
pemanjangan durasi 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.
Gagal jantung akut
Gagal jantung akut:
definisi dan etiologi
Gagal jantung adalah sindrom klinis yang
ditandai dengan gejala khas (misalnya
sesak napas, pergelangan kaki bengkak
dan kelelahan) yang bisa disertai dengan

European Heart Journal. ESC Guidelines for the diagnosis and treatment of
tanda-tanda (misalnya peningkatan
tekanan vena jugularis, crackles paru dan
edema perifer) yang disebabkan oleh

acute and chronic heart failure.2012:33;1842-32

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.

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 • Routine laboratory testing
at rest except for feeling uncomfortable when lying flat for more than a
• Electrocardiogram (ECG)
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 • CXR
dysfunction, the pulse pressure may be diminished, • Assessment of LV function
reflecting a reduction in stroke volume, sinus tachycardia, cool peripheral
extremities and cyanosis of the lips and nail bed • Biomarkers
• Jugular veins  In the early stages of HF, the venous pressure may be • Exercise testing
normal at rest but may become abnormally elevated with sustained (∼1
min) pressure on the abdomen (positive abdominojugular
reflux).
• 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.
 Algoritma Diagnosis

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

European Heart Journal. ESC Guidelines for the diagnosis and treatment of acute and
Rosen’s Emergency Medicine, 9th ed. 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 • Aterosklerotik
secara progresif ke proksimal atau distal dari aorta. • Tumor mediastinal
Lapisan dalam dari dinding aorta mengalami robekan, • Pankreatitis akut
sdgkn lapisan luar utuh  darah mengalir mll robekan
dan membelah lapisan tengah dinding aorta dan
membentuk saluran baru di dalam dinding aorta. • Pemeriksaan:
• Gambaran klinis: • Lab: peningkatan CRP, leukositosis ringan hingga sedang,
dan sedikit peningkatan LDH
• Sakit dada atau punggung dg rasa sakit spt tertusuk benda • Pd ps yg tiba dg onset <24 jam, kadar D-dimer <500ng/mL
tajam
• EKG: hipertrofi ventrikel kiri akibat hipertensi yg lama
• Rasa sakit yg timbul tiba-tiba
• Foto thoraks: pelebaran mediastinum superior, bayangan
• Denyut yg lemah atau tidak ada denyut pd brakialis (pulse ganda dinding aorta, dan perbedaan ukuran aorta asenden
deficit) dan desenden. Kadang adijumpai kardiomegali sekunder
• Hipertensi karena efusi pericardial atau tanda efusi pleura.
• Rasa sakit berpindah-pindah • Retrograde aortography
• Diagnosis: gejala klinis + adanya pelebaran aorta • CT-scan
atau mediastinal pada pemeriksaan radiografi • MRI: sensitivitas 85%, spesifisitas 100%
• Echocardiography
• Diagnosis banding: • Transthoracic echocardiographt (TTE): sensitivitas 60-80%
• Iskemia miokard dan spesifitas 83-96%
• Perikarditis • Transesophageal echocardiography (TEE): spesifisitas 82-
• Emboli paru 95% & sensitivitas 92-100%
• Nyeri otot • Intraoperatif epicardial ekokardiografi enamel epitel (IEE)
• Pleuritis • Intravascular ultrasound (iVUS)
• Kolesistitis
EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.
Diseksi aorta
• Pasien dgn dugaan diseksi aorta akut • Obat yang digunakan untuk terapi medis:
harus dirawat intensif untuk evaluasi • Natrium Nitroprusside
diagnostic segera. • Nitrogliserin
• Morfin sulfat  menghilangkan nyeri • Nikardipin
• Clevidipine
• Beta blocker iv (metoprolol, propranolol, • Fenoldopam
labetalol)  mengontrol target tek darah
sistolik 110 mmHg • Beta Blocker

• Pilihan terapi bedah  untuk Stanford • Tindakan bedah:

tipe A (aorta asendens) • Indikasi : semua pasien dengan diseksi
proksimal dgn pengecualian pasien kondisi
• Pilihan terapi medis  untuk Stanford tipe serius yg menghalangi operasi
B (aorta desenden tmsk diseksi aorta • Teknik yg sering digunakan utk diseksi aorta
abdominal) asenden : Bentall, cabrol, button, elephant
trunk
• Terapi medis:
• Pengobatan antihipertensi secara iv harus • Terapi intervensi pemasangan stent: Hasil
segera dimulai pada semua pasien diseksi dari pemasangan stent menyebabkan
aorta akut kecuali ps hipotensi. perbaikan aliran darah pd pembuluh darah
• Th/ standard saat ini: kombinasi dari beta yg tersumbat akibat diseksi aorta
blocker dan vasodilator (natrium
nitroprusside)
EIMED PAPDI Kegawatdaruratan Penyakit Dalam. Buku 1 EIMED Dasar.
Diseksi aorta
• Komplikasi: dapat menyebabkan oklusi rasa sakit yg hebat, timbulnya syok, deficit
cabang aorta  kerusakan pada organ pulse, dan adanya deifisit neurologis
• Murmur diastolic aorta (50% kasus) karena • Tingkat kelangsungan hidup jangka pjg ps
regurgitasi aorta diseksi aorta proksimal yg menjalani
tindakan bedah: 65-80% pd 5 tahun dan
• Gagal jantung
40-50% pd 10 tahun
• Tamponade jantung
• Penyebab plg umum kematian jangka
• Gejala neurologis dapat ditemukan panjang dari diseksi aorta adl pecahnya
• Pd keterlibatan A. celiac: nyeri perut aorta dan mengakibatkan diseksi
terums-menerus, meningktnya protein berikutnya atau aneurisma.
fase akut, dan peningkatan laktat
dehydrogenase.
• 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