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Pemicu 5

Blok Kegawatdaruratan
Aldi Firdaus
405140098
LI
1. Klasifikasi cardiac vascular emergency
2. ACS
3. Unstable angina
4. Angina pectoris
5. Cor pulmonale
6. Gagal jantung
7. Cardiac arrest
8. Takikardi
9. Krisis hipertensi
LI 1
LI 2
KLASIFIKASI

UNSTABLE ANGINA
PECTORIS (UAP)
PARTIALY
OCCLUDED NON ST ELEVATION
ACUTE MYOCARD INFARCT
CORONARY (NSTEMI)

SYNDROME ST ELEVATION
TOTALLY
MYOCARD INFARCT
OCCLUDED (STEMI)

Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011
ETIOLOGI
Thrombosis arteri
ATEROSKLEROTIK
koroner
ETIOLOGI

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
Acute Coronary Syndromes

Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011
Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011
Lilly LS. Pathophysiology of Heart Disease, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2011
STEMI :
Clinical Presentation
• Precipitating factor  physical exercise,
emotional stress, / a medical / surgical illness
• Pain deep & visceral heavy, squeezing, &
crushing, stabbing / burning
– central portion of the chest &/ the epigastrium,
radiates to the arms
– Occurs at rest  more severe, & lasts longer.
– Pain is not uniformly present in patients w/ STEMI 
painless STEMIs is ↑in patients w/ DM, & ↑ age
• Weakness, sweating, nausea, vomiting, anxiety,
and a sense of impending doom

Harrison’s principles of internal medicine,19th ed. p. 1599-611


STEMI :
Clinical Presentation (2)
• Physical Findings
– Anxious & restless
– Pallor associated w/perspiration & coolness of the extremities
– Substernal chest pain persisting for >30 min
– Diaphoresis
– Normal pulse rate & BP within the 1st hour

• STEMI progresses through the following temporal stages:


(1) acute (first few hours–7 days); (2) healing (7–28 days); &
(3) healed (=29 days).
– When evaluating the results of diagnostic tests for STEMI, the
temporal phase of the infarction must be considered.
Harrison’s principles of internal medicine,19th ed. p. 1599-611
STEMI :
Laboratory Findings
• ECG

• Cardiac Imaging
– Two-dimensional echocardiography
– Radionuclide imaging techniques  rare
– high-resolution cardiac MRI

Rosen’s emergency medicine, 8th ed. p. 997-1033


Harrison’s principles of internal medicine,19th ed. p. 1599-611
DIAGNOSIS ACS

SPECIFIC SERUM
ACUTE ECG MARKERS OF
SYMPTOMS
ABNORMALITIES MYOCARDIAL
NECROSIS

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

Rosen’s emergency medicine, 8th ed. p. 997-1033


TATALAKSANA

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

ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation
TATALAKSANA STEMI

Fibrinolitik Dosis
Streptokinase 1,5 juta unit lebih dari 30-60 menit
Alteplase 15 mg bolus,
(rt-PA) dilanjutkan 0,75 mg/kg (maks 50 mg) lebih dari 30 menit
Dilanjutkan 0,5 mg/kg (maks 35 mg lebih dr 1 jam
Reteplase 10 U bolus 2kali interval 30 menit
(r-PA)
Tenecteplase Berdasarkan BB
(TNK-PA) <60 kg, 30 mg
60-69, 35 mg
70-79, 40 mg
80-89, 45 mg
> 90, 50 mg

IPD hal 1457-1466


Penyekat beta Dosis awal Dosis target
Bisoprolol 1 x 2,5 mg Sampai 1 x 10 mg
Metoprolol 2-4 x 25 mg Sampai 2-4 x 50 mg, lalu titrasi turun
Carvedilol 2 x 6,25 mg Sampai 2 x 25 mg

ACE inhibitor Dosis awal Dosis target


Captopril 3 x 6,25 mg Sampai 3 x 25 – 50 mg
Ramipril 2 x 2,5 mg Sampai 2 x 5 mg
Lisinopril 1 x 2,5 – 5 mg Sampai 2 x 10 - 20 mg
Enalapril 1 x 2,5 – 5 mg Sampai 1 x 10 mg
Perindopril 1 x 2,5 mg Sampai 1 x 5 mg
Trandolapril 1 x 0,5 mg Sampai 1 x 4 mg

ARB Dosis awal Dosis target


Losartan 1 x 12,5 mg Sampai 1 x 50 mg
Valsartan 2 x 20 mg/hari Sampai 160 mg/hari
• Kontraindikasi absolut : – Riwayat trauma dalam 1
– Riwayat stroke hemoragik bulan terakhir termasuk
dalam 1 tahun terakhir cidera kepala atau resusitasi
jantung > 10 menit atau
– Neoplasma intrakranial riwayat operasi mayor dalam
– Perdarahan internal yg aktif kurang dari 3 minggu
– Kecurigaan adanya diseksi – Riwayat terapi streptokinase
aorta sebelumnya
• Kontraindikasi relatif – Riwayat alergi dengan
– Hipertensi berat yaitu streptokinase
tekanan darah > 180/110 – Hipertensi kronik berat
mmHg – Resusitasi yg gagal
– Dalam terapi antikoagulan
oral
– Riwayat perdarahan internal
dalam 4 minggu terakhir
– Kehamilan
– Tukak lambung aktif
NSTEMI
Iskemi atau infark miokard akibat reduksi dari aliran darah coroner
Definisi tanpa elevasi segmen ST diikuti kenaikan biomarker (troponin maupun
CK-MB)

Ketidakseimbangan antara myocardial oxygen consumption (MVO2) dan


Etiologi
demand yg diakibatkan obstruksi arteri coroner

• Histori gejala:
• Nyeri dada seperti ditekan saat istirahat atau dengan minimal 10
menit
Diagnosis • Sering dimulai dari retrosternal dan dapat menjalar ke lengan kiri
(sering) dan kanan, leher
• Disertai diaphoresis, dyspnea, nausea, abdominal pain, atau
syncope

2014 AHA/ACC Guideline for the


Management of Patients With Non–ST-
Elevation Acute Coronary Syndromes
NSTEMI
Lanjutan • Pemeriksaan fisik
diagnosis • Disfungsi ventricular  terdapat S4
• Split paradoksikal bunyi jantung kedua
• Dapat ditemukan murmur regurgitasi mitral akibat disfungsi
otot papilaris
• EKG
• Depresi segmen ST yg baru menunjukan iskemia akut
• New T-wave inversion
• 1-6% EKG normal
• Biomarker
• Tropnin T atau I positif dalam beberapa jam setelah onset dan
bertahan smpai 2 minggu
• CK-MB kurang spesifik karna ada d otot skeletl juga (beberapa
jam sampai 48 jam)

2014 AHA/ACC Guideline for the


Management of Patients With Non–ST-
Elevation Acute Coronary Syndromes
Tatalaksana Awal RS
Oksigen Bila saturasi O2 <90%, respiratory distress atau high risk
hypoxemia
Nitrogliserin Sublingual 0,4 mg, dapat diberikan 3 dosis interval 5 menit
(NTG) (mengurangi nyeri dada dan dilatasi PD ↓preload &
↑suplai  ↓kebutuhan O2 miokard

Analgesic Morfin  Mengurangi nyeri


therapy 1-5 mg IV, dapat diulang interval 5-30menit maks 20 mg

Aspirin Aspirin bukkal 160-325 mg di ruang emergency


Lanjutan: oral 75-162 mg

2014 AHA/ACC Guideline for the


Management of Patients With Non–ST-
Elevation Acute Coronary Syndromes
Tatalaksana Awal
Beta blocker IV Metoprolol 5 mg setiap 2-5 menit sampai 3 dosis
jika HR>60, sistol>100, PR interval <0,24 dan ronki<10cm
dr diafragma
Lanjutan : oral metoprolol 50 mg tiap 6 jam selama 48
jam dan dilanjutkan 100 mg tiap 12 jam
CCB Berikan bila:
• Beta blocker tidak berhasil
• Reccurent iskemi, KI beta blocker, resiko syok
kardiogenik, PR interval >0,24
Co:verapamil atau diltiazem
Cholesterol management

2014 AHA/ACC Guideline for the


Management of Patients With Non–ST-
Elevation Acute Coronary Syndromes
http://eurheartj.oxfordjournals.org/content/ehj/early/2015/08/28/eurheartj.ehv32
Tatalaksana

2014 AHA/ACC Guideline for the


Management of Patients With Non–ST-
Elevation Acute Coronary Syndromes
LI 3
Angina
• Definition
– Stable angina
• chest or arm discomfort that may not be described
as pain but is reproducibly associated with physical
exertion or stress and is relieved within 5–10 min
by rest and/or sublingual nitroglycerin
– Unstable angina
• equivalent ischemic discomfort + 1 of 3 features:
– occurs at rest (or with minimal exertion), lasting >10 min
– severe and of new onset (within the prior 4–6 weeks)
– occurs with a crescendo pattern
Unstable Angina
• Pathophysiology
– oxygen supply < +/ myocardial oxygen demand > +
atherosclerotic coronary plaque
• plaque rupture or erosion with superimposed
nonocclusive thrombus
• dynamic obstruction (coronary spasm, as in
Prinzmetal's variant angina)
• progressive mechanical obstruction (rapidly advancing
coronary atherosclerosis)
• UA secondary  myocardial oxygen demand and/or
decreased supply (tachycardia, anemia)
Unstable Angina
• History & physical examination
– chest pain (substernal region or sometimes in the
epigastrium  radiates to the neck, left shoulder,
and left arm)
– Diaphoresis
– pale cool skin
– sinus tachycardia
– basilar rales
– sometimes hypotension
Unstable Angina
• Electrocardiogram
– ST-segment depression, transient ST-segment
elevation, and/or T-wave inversion  30-50%
• Cardiac biomarkers
– CK-MB and troponin >
• minor troponin elevations have been reported and can
be caused by congestive heart failure, myocarditis, or
pulmonary embolism  false positive value
Unstable Angina
• Short term management
– placed at bed rest with continuous ECG
monitoring for ST-segment deviation and cardiac
rhythm
– Ambulation is permitted if
• patient shows no recurrence of ischemia (discomfort or
ECG changes)
• does not develop a biomarker of necrosis for 12–24 h
– Medical therapy
• Anti-ischemic & anti-thrombotic treatment
Unstable Angina
– Anti-ischemic therapy
• Include bed rest, nitrates, beta blockers
• Nitrates
– sublingually or by buccal spray (0.3–0.6 mg)
– Persist after three doses given 5 min apart  IV nitroglycerin
(5–10 ug/min using nonabsorbing tubing)  may be
increased by 10 ug/min every 3–5 min  pain relieved or
systolic arterial pressure <100 mmHg
– pain-free for 12–24 h  Topical or oral nitrates replace the IV
nitroglycerin
• Beta blockers
– IV followed by oral beta blockers  heart rate of 50–60
beats/min
Unstable Angina
– Antithrombotic therapy
LI 4
Angina Pectoris
• Is transient, episodic chest discomfort resulting from
myocardial ischemia.
• This discomfort predictable and reproducible  with the
frequency of attacks constant
• RF  Physical or psychological stress (physical exertion,
• Emotional stress, anemia, dysrhythmias, or environmental
exposures)
• May provoke an attack of angina that resolves spontaneously
over a constant, predictable period of time with rest or
nitroglycerin (NTG).

Rosen 8th Edition Page 1000


Angina Pectoris
• Canadian Cardiovascular Society classification :
– class I, no angina with ordinary physical activity
– class II, slight limitation of normal activity as angina occurs
with walking, climbing stairs, or emotional stress
– class III, severe limitation of ordinary physical activity as
angina occurs on walking one or two blocks on a level
surface or climbing one flight of stairs in normal conditions
– class IV, inability to perform any physical activity without
discomfort as anginal symptoms occur at rest

Rosen 8th Edition Page 1000


Angina Pectoris
• Heaviness
• Pressure
• Squeezing
• Anginal pain  burning and aching.
• Some patients absence pain  but dyspnea or a vague sense of
anxiety.
• The location usually retrosternal
• Most do not localize the pain to any small area.
• Discomfort may radiate to the neck, jaw, teeth, arms, or shoulders,
reflecting the common origin in the posterior horn of the spinal
cord of sensory neurons supplying the heart and these areas.
• Occasional patients report epigastric distress with ischemic episode

Harrison 16th Edition Page 77


Angina Pectoris

Harrison 16th Edition Page 77


Harrison 16th Edition Page 77
Lange Clinical Emergency Medicine Edition
LI 5
Acute Cor Pulmonale
Etiology Cor pulmonale is a state
of cardiopulmonary dysfunction
that may result from several
different aetiologies and
pathophysiologic mechanisms
(table I):
• Pulmonary vasoconstriction
(secondary to alveolar hypoxia or
blood acidosis).
• Anatomic reduction of the
pulmonary vascular bed
(emphysema, pulmonary emboli,
etc.)
• Increased blood viscosity
(polycythaemia, sickle-cell
disease, etc.)
• Increased pulmonary blood flow

http://medind.nic.in/jac/t04/i2/jact04i2p128
Symtomps Evaluation
• Fainting spells during • Chest radiography
activity • Electrocardiography
• Chest discomfort, usually in • Two dimensional and Doppler
the front of the chest echocardiography (which can
provide an indirect
• Chest pain
measurement of pulmonary
• Swelling of the feet or artery pressure when tricuspid
ankles regurgitation is present)
• Symptoms of lung disorders, • Pulmonary function tests
such as wheezing or • Radionuclide ventriculography
coughing • Magnetic resonance imaging
• Bluish lips and fingers • Right heart catheterisation
(cyanosis) • Lung biopsy

https://medlineplus.gov/ency/article/000129.htm http://medind.nic.in/jac/t04/i2/jact04i2p128
LI 6
Chronic
heart failure

https://heartfoundation.org.au/images
/uploads/publications/CHF-QRG-
updated-2014.pdf
https://heartfoundation.org.au/images/upload
s/publications/CHF-QRG-updated-2014.pdf
https://heartfoundation.org.au/images/upload
s/publications/Chronic_Heart_Failure_Guidelin
es_2011.pdf
Algorithm
for CHF

https://heartfoundation.org.au/ima
ges/uploads/publications/CHF-QRG-
updated-2014.pdf
https://heartfoundation.org.au/images/upload
s/publications/CHF-QRG-updated-2014.pdf
https://heartfoundation.org.au/images/upload
s/publications/Chronic_Heart_Failure_Guidelin
es_2011.pdf
https://heartfoundation.org.au/images/upload
s/publications/Chronic_Heart_Failure_Guidelin
es_2011.pdf
Main side-
Vasodilator Indication Dosing Other
effects
Pulmonary Start 10–20
Tolerance on
Nitroglycerin congestion/oe µg/min, Hypotension,
continuous
e dema BP >90 increase up to headache
use
mmHg 200 µg/min
Pulmonary Start with 1
Tolerance on
Isosorbide congestion/oe mg/h, Hypotension,
continuous
dinitrate dema BP >90 increase up to headache
use
mmHg 10 mg/h
Hypertensive
Start with 0.3
HF Hypotension,
Nitroprussid µg/kg/min and Light
congestion/oe isocyanate
e increase up to sensitive
dema BP >90 toxicity
5 µg/kg/min
mmHg
Pulmonary
Bolus 2 µg/kg
congestion/oe
+ infusion
Nesiritide* dema Hypotension
0.015–0.03
BP >90
µg/kg/min
Daily dose
Fluid retention Diuretic Comments
(mg)
Oral or i.v. according to clinical
Moderate Furosemide or 20–40
symptoms
Titrate dose according to clinical
bumetanide or 0.5–1
response
Monitor K, Na, creatinine, blood
torasemide 10–20
pressure
Severe Furosemide 40–100 i.v. Increase dose
Furosemide (5–40
Better than very high bolus doses
infusion mg/h)
Bumetanide 1–4 Oral or i.v.
Torasemide 20–100 Oral
Add
Refractory to loop Combination better than very high
hydrochlorothia 50–100
diuretic dose of loop diuretics
zide
More potent if creatinine clr < 30
or metolazone 2.5–10
ml/min
or Spironolactone best choice if no
25–50
Bolus Infusion rate
Dobutamine No 2–20 µg/kg/min (β+)
<3 µg/kg/min: renal
effect (δ+)
3–5 µg/kg/min: inotropic
Dopamine No
(β+)
>5 µg/kg/min: (β+),
vasopressor (α+)
25–75 µg/kg over 10-20
Milrinone 0.375–0.75 µg/kg/min
min
Enoximone 0.25–0.75 mg/kg 1.25–7.5 µg/kg/min
0.1 µg/kg/min which can
12 µg/kg over 10 min be decreased to 0.05
Levosimendan*
(optional)** or increased to 0.2
µg/kg/min
Norepinephrine No 0.2–1.0 µg/kg/min
Bolus: 1 mg can be
LI 7
CARDIAC ARREST
Cardiac electrical conduction

Step 1: Pacemaker Impulse Generation


Step 2: AV Node Impulse Conduction
Step 3: AV Bundle Impulse Conduction
Step 4: Purkinje Fibers Impulse
Conduction

The heart muscle contracts

pulse, blood pressure, breathing &other signs of circulation


Cardiac arrest
• SCD (sudden cardiac death) is a direct
consequence of cardiac arrest, which may be
reversible if responded to promptly. Since
resuscitation techniques and emergency
rescue systems are available to respond to
victims of out-of-hospital cardiac arrest, which
was uniformly fatal in the past, understanding
the SCD problem has practical importance
Cardiac arrest from a primary
cardiac origin typically presents as:
• VF  old MI, acute MI
• VT  miocardial hypertrophy, cardiomiopathy, specific
structural abnormalities
• PEA
• Asystole

• Metabolic  hyperalemia  result in progressive


widening of the QRS complex  can deteriorate to VT,
VF, asystole or PEA.
• Electrocution
• Primary respiratory failure  initial
hypertension and tachycardia 
progressing through bradycardia to PEA,
VF or asystole.

Cardiopulmonary arrest is defined by the


triad of unconsciousness, apnea, and
pulselessness.
Physical Examination
Physical examination of a cardiac arrest patient
is necessarily focused on a few key goals:
• (1) ensure adequacy of airway maintenance
and ventilation,
• (2) confirm the diagnosis of cardiac arrest,
• (3) find evidence of cause, and
• (4) monitor for complications of therapeutic
interventions.
Management
• Resuscitation (CPR)
• Defibrillation
Monitoring
• Arterial Blood Pressure and Coronary
Perfusion Pressure
• End-tidal Carbon Dioxide
• Central Venous Oxygen Saturation
• Echocardiography
• Laboratory Testing
Signs of cardiac arrest
• Sudden loss of responsiveness
• No normal breathing
Post–cardiac arrest care algorithm.

Peberdy M A et al. Circulation 2010;122:S768-S786

Copyright © American Heart Association


LI 8
Aritmia yg mengancam kehidupan
Ventrikel takikardi
– Frekuensi = 100-250 x/mnt
– Irama = tidak teratur
– Gel.P = tdk ada hub gel P dgn QRS (AV disosiasi)
– PR interval = tidak kelihatan
– Lebar QRS = > 0,25 dtk,morfologi berbeda dgn
biasa,bila da multifokal = QRS kompleks akan
terlihat berbeda-beda
Ventricular Fibrillation

• The heart's electrical


activity becomes
disordered  the heart's
lower (pumping) chambers
contract in a rapid,
unsynchronized way. (The
ventricles "flutter" rather
than beat.) pumps little
or no blood  Collapse 
sudden cardiac arrest
Etiology
• Coronary artery disease
• Acute coronary syndromes
• Electrocution
• Drug toxicity and sensitivity
• Asphyxia
• Drowning
Symptoms and Diagnosis
• Ventricular fibrillation causes unconsciousness in seconds.
• seizures and develops irreversible brain damage
(after about 5 minutes because oxygen no longer reaches the brain)
• suddenly collapses
• dilated pupils
• no detectable pulse, heartbeat, or blood pressure.
• Ventricular fibrillation is diagnosed as the cause of the
cardiac arrest by electrocardiography (ECG).
Pulseless electrical activity (PEA)
Etiology
The H’s include: The T’s include:
• Hypovolemia •Toxins
•Tamponade(cardiac)
• Hypoxia
•Tension pneumothorax
• Hydrogen ion (acidosis) •Thrombosis (coronary
• Hyper-/hypokalemia and pulmonary)
• Hypothermia. •Trauma
.
Gambaran EKG
• Kompleks QRS melebar dengan frekuensi
rendah  20-40x/menit atau < 20x/menit
• Irama idioventrikuler
• Asistol  garis lurus tanpa aktivitas ventrikel
(tidak tampak kompleks QRS)
Asystole
• cardiac stand still with no cardiac output and no
ventricular depolarization
• Asystole is sometimes referred to as a “flat line.”
LI 9
HYPERTENSIVE EMERGENCIES
• Hypertensive emergency 
acute elevation in BP (≥180/
110mmHg) associated with
active end-organ damage,
specifically ongoing injury to
the brain, heart, aorta,
kidneys, and/or eyes.

• Most hypertensive
emergencies occur in patients
with chronic HTN

Clinical emergency medicine, Lange. p. 75-9 Rosen’s emergency medicine, 8th ed p. 1116-23
Hypertensive Emergencies :
Clinical Presentation
• History
– Anamnesis  evidence of end-organ damage
– Comprehensive review of systems  presents chest pain, back pain,
shortness of breath, hematuria ↓urine output, & neurologic
complaints
• Physical Examination
– Verifying that the ↑BP
– Perform a detailed physical exam  neurologic, cardiac, pulmonary, &
abdominal examinations
• Diagnostic Studies
– ECG  suspicion for acute cardiac ischemia.
– Laboratory  identify end-organ (urinalysis, BUN, creatinine,
pregnancy test, cardiac enzymes)
– Imaging  head CT, CXR, CT angiography
Rosen’s emergency medicine, 8th ed p. 1116-23
Clinical emergency medicine, Lange. p. 75-9
Hypertensive Emergencies :
Clinical Presentation (2)

Clinical emergency medicine, Lange. p. 75-9


Clinical emergency
medicine, Lange. p. 75-9
Clinical emergency medicine, Lange. p. 75-9
Krisis Hipertensi
• Peningkatan kritis tekanan darah → TDD > 120
mmHg
– Tidak harus demikian → derajat keparahan
gambaran klinis tidak hanya ditentukan angka
absolut tekanan darah → dipengaruhi juga oleh
besar dan laju kenaikan tekanan darah serta
kondisi yang mendasari
• 2 jenis :
– Hypertensive emergencies
– Hypertensive urgencies
Migneco A, Ojetti V, Lorenzo AD, Silveri NG,
Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
HYPERTENSIVE EMERGENCY
• Krisis hipertensi + kerusakan organ akut /
progresif yang mengancam nyawa :
– ACS
– Gagal ventrikel kiri akut dengan edema paru
– Eklamsia
– Diseksi aorta
– Gagal ginjal akut
– Ensefalopati hipertensif
– Stroke iskemi / hemoragik
Migneco A, Ojetti V, Lorenzo AD, Silveri NG,
Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
HYPERTENSIVE URGENCY
• Krisis hipertensi tanpa kerusakan organ akut /
progresif
• Tekanan darah harus diturunkan dalam 24 –
48 jam → cegah kerusakan organ akut dan
baru
• JNC VII → hipertensi stage II batas atas +
gejala (sakit kepala, pusing, ansietas berat,
epistaksis, napas pendek)
Migneco A, Ojetti V, Lorenzo AD, Silveri NG,
Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
ETIOLOGI KRISIS HIPERTENSI

Migneco A, Ojetti V, Lorenzo AD, Silveri NG,


Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
PATOFISIOLOGI KRISIS HIPERTENSI
• Kompleks dan belum diketahui seluruhnya
• Diduga : ↑ resistensi vaskuler mendadak
(dipicu oleh pelepasan zat-zat vasodinamik
seperti NE, angiotensin II) → dekompensasi
dan kerusakan endotel → peningkatan
tekanan darah; sekresi molekul proinflamasi
dan adhesi
• Siklus tersebut berulang
Migneco A, Ojetti V, Lorenzo AD, Silveri NG,
Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
KRISIS HIPERTENSI
MANIFESTASI KLINIS DIAGNOSIS
• Asimtomatik s/d gejala • Anamnesis → riwayat
spesifik yang menunjukkan penyakit
kerusakan organ akut • Status medis
(misal: dispnea, nyeri dada, • Penunjang → EKG,
kelainan neurologis) funduskopi, laboratorium

Migneco A, Ojetti V, Lorenzo AD, Silveri NG,


Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
TATALAKSANA
HYPERTENSIVE EMERGENCY
• ↓ tekanan darah dengan terapi intravena → efek
cukup cepat, timbul dalam jangka waktu yang
terukur
– ↓ tekanan darah secara bertahap → ↓ risiko
hipoperfusi / iskemi organ (serebral, pembuluh
koroner, ginjal)
– ↓ tekanan darah ± 25% dalam beberapa menit. Target
dalam 2 – 6 jam : 160/100 mmHg → dinormalkan
dalam 24 – 48 jam selanjutnya
Pengecualian : pasien diseksi aorta dan edema paru →
segera turunkan ke normal
Migneco A, Ojetti V, Lorenzo AD, Silveri NG,
Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
TATALAKSANA HYPERTENSIVE
EMERGENCY

Migneco A, Ojetti V, Lorenzo AD, Silveri NG,


Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
TATALAKSANA HYPERTENSIVE
EMERGENCY

Migneco A, Ojetti V, Lorenzo AD, Silveri NG,


Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
TATALAKSANA
HYPERTENSIVE URGENCY
• ↓ tekanan darah dalam 24 – 48 jam dengan terapi
peroral
• Pilihan disesuaikan dengan riwayat medis dan
penyakit kronis yang mendasari

Migneco A, Ojetti V, Lorenzo AD, Silveri NG,


Savi L. Hypertensive crises: diagnosis and
management in the emergency room. Eur
Rev Med Pharmacol Sci. 2004;8:143-52.
Katzung BG, Masters SB, Trevor AJ, editors.
Basic & clinical pharmacology. 12th ed.
New York: The McGraw-Hill Companies,
Inc.; 2012.