Dr.

DANI ROSDIANA, SpPD

Bag Penyakit Dalam FK UNRI

Melakukan prosedur kedaruratan klinis

Menentukan keadaan kedaruratan klinis

Memilih prosedur kedaruratan klinis sesuai

kebutuhan pasien atau menetapkan rujukan

Melakukan prosedur kedaruratan klinis secara

benar dan etis, sesuai dengan kewenangannya

Mengevaluasi dan melakukan tindak lanjut

Keluhan utama

Survey primer,
Survey sekunder
PROBLEM
EMERGENCY?

PROSEDUR
KEDARURATAN

CARDIOVASCULAR

1. Heart

failure
2. Acute Myocard infarction
3. Cardiorespiration arrest
4. Arythmia : atrial flutter, Supraventricular
tachycardia, Ventricular extrasystole
Aorta-arteries disorders
1. Hypertension
2. Hypovolemic shock
3. Septic shock

LUNG
1. TB paru
2. Bronchial asthma
3. Status asmaticus
4. Atelectasis
5. SARS
6. Pneumonia

STOMACH & DUODENUM

1. Gastric/duodenal ulcer
2. Gastrointestinal bleeding/HEMATEMESIS
3. Peritonitis

LIVER, GALL BLADDER

1. Amoebic liver abscess
2. Liver failure
3. Acute cholesystitis

NEPHROLOGY
1. Acute Renal failure
2. Complicated Chronic renal failure

ENDOCRINOLOGY DISORDER
1. Complication of DM
2. Hypoglycemia
3. Adrenal cortex failure

ERROR OF METABOLISM
1. Gout

INFECTION
1. Cerebral malaria
2. HIV AIDS
3. Tetanus
4. Rabies
5. Avian flu
6. Pertusis

AIRWAY?
BREATHING?
CIRCULATION
DRUG
EXPOSURE

PROBLEM GAWAT
DARURAT ?

PENANGANAN
AWAL

PERENCANAAN
RUJUKAN

ASMA
FEBRIS: DHF, DSS
CHF
CKD
KOMA HIPOGLIKEMIA, HIPERGLIKEMIA
HIPERTENSI
PPOK
KESADARAN MENURUN
HEMATEMESIS MELENA, HEMATOSCESIA,
PALPITASI, ARITMIA

Dyspnea
PARU?
Asma ?
PPOK ?
Pneumonia?
TB paru?
Pneumothorak?
Bronchiectasis ?

JANTUNG?

GINJAL? HEPAR?

Hipertensi
Emergensi?
Gagal ginjal
akut?
Gagal ginjal
kronik?

Gagal jantung?
Aritmia?
Infark
miokard?

METABOLIS
ME?
Asidosis
metabolik?
DD : KAD/HONK
CKD
Krisis tiroid?

Gagal
hati/decompen
sasi

Acute Coronary Syndrome

ST Elevation

No ST Elevation
Non ST Elevation MI

Unstable
Angina

Myocardial Infarction
Non Qw MI

Braunwald E et al. J Am Coll Cardiol 2000;

36:970-1062

Qw MI

Pathophysiology of ACS: Disrupted

Plaque
Thin cap

High
macophage
content

Complete
coronary
occlusion

Incomplete
coronary
occlusion

Spontaneous lysis
repair, and wall remodelling

Large lipid core

Acute
MI

Temporary
resolution of
instability
Future high-risk
lesion

Adapted from Yeghiazarians et al. N Eng J Med, 2000;

342:101-114

Unstable
angina
or non-Q-wave
MI

Guidelines for the Identification of ACS Patie

Chief Complaint
Chest pain typical of myocardial ischemia
or MI
Associated : dyspnea, nausea and/or
vomiting
diaphoresis
Medical History
CABG, angioplasty, CAD, angina on effort,
or AMI
NTG use to relieve chest discomfort
Risk factors
Special Considerations

Pathophysiology of coronary heart

disease
Mechanisms of myocardial ischaemia
O2
transport
capacity

Contractili
ty
Heart rate

O2
consumptio
n

O2
supply

Wall
stress
Ventri
cular
volum
e

Wall
thick
ness

LV enddiastoli
c
pressur
e

Angina
pectoris

Coronary
blood flow

ISCHAEMI
A
ST segment
depression
- elevation

Impaired
perfusion
Metabolic
changes

Arterial
O2 saturation
Haematocrit
Diastolic aortic
pressure
Coronary
vascular
resistance
Coronary
spasm
Organic
stenosis
Impaired
pump
function

Angina
Pektoris
Tidak Stabil
Rawat di Ruang Rawat
Intensif
Obat-obat:
Penyekat
Aspirin
beta
Heparin
Antagonis
Nitrat
kalsium

Stabil dan bebas sakit dada

Stop Heparin, Mobilisasi, Tentukan fungsi
Vki

Tidak stabil dan sakit menetap >

48 jam
Angiografi koroner kalau perlu dengan
PBIA

Disfungsi Vki sedang

berat
Tida
k

Ya

Angiogra
f
Koroner

AK/BP
K

ULJB
Risiko
rendah

Risiko
tinggi

Pulangkan, terapi, aspirin dan antiangina, evaluasi berkala,

pencegahan sekunder

Stratifikasi risiko dan tata laksana pengobatan angina tak

stabil. (RSJHK, 1999)

Dyspnea
PARU?
Asma ?
PPOK ?
Pneumonia?
TB paru?
Pneumothorak?
Bronchiectasis ?

JANTUNG?

GINJAL? HEPAR?

Hipertensi
Emergensi?
Gagal ginjal
akut?
Gagal ginjal
kronik?

Gagal jantung?
Aritmia?
Infark
miokard?

METABOLIS
ME?
Asidosis
metabolik?
DD : KAD/HONK
CKD
Krisis tiroid?

Gagal
hati/decompen
sasi

Kesadaran menurun

STRUKTURAL

Stroke : hemoragik?
non hemoragik?
Trauma?

GANGGUAN METABOLIK

Koma hipoglikemik
Koma hiperglikemik
Koma hepatikum
Koma uremikum
Syok : septik?
Hipovolemik?,
cardiogenik?
Survey primer dan
survey sekunder

Otak dalam keadaan normal :

butuh 50% produksi glukosa basal
( 1 mg/kg/menit )
Kerusakan otak tergantung dari
lama, berat, cepat
Bila Hipoglikemia akan merusak

korteks serebri
hipokampus
batang otak /spinal bebas.
Bila Hipoksia menyebabkan

neuropati sensorimotor perifer

Aktivasi saraf otonom :

Berdebar, lapar, gemetar, keringat dingin, nausea
Neuro-glycopenia :
Mengantuk, perilaku aneh, sukar konsentrasi
inkoordinasi, sulit bicara.
Akibat berat :
hemiparesis, konvulsi, chore-atetosis
ataxia, dekortikasi.

Penanganan hipoglikemia
Glukosa :
kalori reaksi cepat , oral/parenteral
D40% 2 fls lanj dengan D 10%
Glukagon 1 mg i.m
adrenalin ( bukan CS )
Infus D5 diberikan selama 1 2 hari
Belum sadar ??
Pikirkan penyebab lain

DD:
Variseal : pecahnya varises esofagus
Non variseal: gastritis erosif, mallory weiss
syndrom, carsinoma dll gaster, esofagitis

Penatalaksanaan:
1. Airway
2. Oksigenasi
3. Circulasi: infus line : cairan yang cukup
tanda-tanda syok hipovolemik??
4. Ngt
5. Inj Somatostatin :
6. Inj PPI
7. Transfusi:

DEFINITION :

HYPERTENSIVE CRISIS
A severe elevation in BP, generally a SBP > 220 mm Hg and / or
DBP > 120 mm Hg. (JNC-VI, 1997)

HYPERTENSIVE EMERGENCIES
Severe elevation in BP complicated by acute target organ
dysfunction, such as coronary ischemia, stroke, intracerebral
hemorrhage, pulmonary edema, or acute renal failure.

HYPERTENSIVE URGENCIES
Severe elevations in BP without evidence of target organ
deterioration.

Colhum DA. Oparil S, New Engl. J. Med, 323 : 1177, 1990

HYPERTENSIVE CRISIS
DBP >120 mmHg

URGENCY

EMERGENCY

BP within hours < 24 hours

BP within minutes < 1 hours

(PARENTERAL / ORAL)

KAPLAN NM . Lancet 344:1335,1994

(PARENTERAL)
-

Accelerated malignant hypertension

Hypertensive encephalopathy
Intracerebral/Subarachnoid hemorrhage
Acute aortic dissection
Acute left ventricular failure
Acute myocardial infarction
Acute glomerulonephritis
Eclampsia

PATHOPHYSIOLOGY

Critical Degree of Hypertension

Local Effects
(Prostaglandins, Free Radical, etc.

Systemic Effects
(Renin-angiotensin, Cathecol,
Vasopression

Endothelial Damage
Pressure Natriuresis
Platelet Deposition
Hypovolemia

Mitogenic and Migration

Factors

Further Increase in
Vasopressure

Myointimal Proliferation

Further Rise in Blood Pressure

And
Vascular Damage
Tissue Ischemia
M. Kaplan, Clinical Hypertension, 7th edition, Baltimore, 266
: 1998

Initial Evaluation of Patients with a Hypertensive

Emergencies
HISTORY

Prior diagnosis and treatment of hypertension.

Intake of pressor agent : street drugs, sympathomimetics.
Symptom of cerebral, cardiac, and visual dysfunction.

PHYSICAL EXAMINATION

Blood Pressure
Funduscopy
Neurologycal Status
Cardiopulmonary status
Body fluid volume assessment
Peripheral pulses

LABORATORY EVALUATION

Packed cell volume and blood smear

Urine analysis
Chemistry : creatinine, glucose, electrolytes
Electrocardiogram
PRA and aldosterone (if primary aldosteronism is suspected)
PRA before and 1 hour after 25 mg Captopril (if renovascular hypertension is
suspected).
Spot urine for metanephrine (if pheochromocytoma is suspected)
Chest radiograph (if heart failure or aortic dissection is suspected)
M. Kaplan, Clinical Hypertension, 7th edition, Baltimore, 267 :

Treatment
1. The goal of therapy is to reduce systemic vascular
resistance.
2. The approach is to initially reduce mean arterial pressure
by about 25 % with further reductions accomplished more
gradually.
3. In general the initial reduction should be achieved over a
period of 1 to 2 hours with less rapid reduction over the
ensuring 6 hours to a DBP of + 100 mm Hg.
4. With the exception of patients with aortic dissection, the
BP should not be reduce to normotensive and especially
hypotensive levels, as target organ hypoperfusion may
results.

Hypertension in the setting of acute

ischemic stroke should only be treated
rarely and cautiously .
Treat : DBP > 120-130 mmHg , objective
reduction 20 % in the frst 24 hours.
Abandon oral nifedipine.
Short actingIV.
(labetalol,nicardipine,fenoldopam )
SNP increase ICP,cyanide poisoning

Hypertension serve to protect CBF in the

setting of high ICP.
Treat if : systolic blood pressure > 200
mmHg or DBP > 110 mmHg.
The rate of decline in blood pressure was
independently associated with increased
mortality.

Intravenous Drugs
for Hypertensive
Emergency
DRUGS

DOSAGE

ONSET of ACTION

Nitropruside

0.25 10 g/kg/min as IV Infusion

Instantaneous

Nitroglycerin

5 100 g/min as IV Infusion

2 5 min

Nicardipine

5 15 mg/hours IV

5 10 min

Hydralazine

10 20 mg IV

10 20 min

10 50 mg IM

20 30 min

1.25 5 mg q 6 hours

15 min

0.1 0.3 g/kg/min

< 5 min

5 15 mg IV

1 2 min

Esmolol

500 g/kg/min for 4 min, then 150

300 g/kg/min IV

1 2 min

Labetolol

20 80 mg IV bolus every 10 min

2 mg/min IV Infusion

5 10 min

Enalapril
Fenoldopam
Phentolamine

Braunwald , 2001

Intravenous Drugs for Hypertensive

Emergencies Available in Indonesia

Vasodilators
Clonidine
Nitroglicerin
Sodium Nitropruside
Ca-Antagonist
Diltiazem Hydrochloride

COMMONLY USED DRUG IN

HYPERTENSIVE EMERGENCY

DILTIAZEM I.V. (HERBESSER)

Useful for hypertensive emergency and urgency.
Acts as calcium slow-channel blockers.
Dose-dependent :

Predictable onset of action

Rapidly reduced BP.

No rebound on withdrawn

Adverse effect : bradycardia, hypotension, headache, flushing.

Has antiischemic and antiarrhythmic effect (class-IV)

DILTIAZEM-Injection

Dosage and Administration

Each
Eachampoule
ampouleof
ofDILTIAZEM-Injection
DILTIAZEM-Injectionshould
shouldbe
bedissolve
dissolvein
in
at
atleast
least55mL
mLaquadest
aquadestor
orNaCl
NaClor
orglucose
glucosesolution
solutionbefore
beforeuse.
use.

BOLUS I.V. INJECTION

0.20 0.35 mg/kg BW
Adult (50kg) : 1 Ampoule (1 3 minutes)
DRIP I.V. INFUSION (Flat)
5 15 mcg/kg BW/min
Adult (50kg) : 15mg/hour 45 mg/hour
DRIP I.V. INFUSION (maintenance)
1 5 mcg/kg BW/min
Adult (50kg) : 5mg/hour 15 mg/hour

Bolus I.v.
0.2 mg/kg
10

10% MBP reduction

From Baseline

20

20% MBP reduction

From Baseline

30

Target MBP
Level

Drip infusion
50 mg/hour

Drip infusion
30 mg/hour

Drip infusion
5-10 mg/hour
Every 30-60 minutes observation
Switch to Oral
DILTIAZEM 180SR

COMMONLY USED DRUG IN

HYPERTENSIVE EMERGENCY
CLONIDINE I.V.
Reduce peripheral sympathetic tone by central
stimulation of 2- receptor.
Unpredictable onset of action.
Adverse effect : sedation, dry mouth, constipation
and a tendency to a overshoot or rebound hypertension
on withdrawn.
W.H. Frishman, et al., Cardiovascular Pharmacotherapy, 1996

COMMONLY USED DRUG IN

HYPERTENSIVE EMERGENCY
NITROGLISERIN I.V.

Strongth vasodilator (arterial- and veno-dilator).

Direct interacting with nitrate receptors on vascular

smooth muscle.

A rapid onset and duration of action.

Adverse effect : headache, tachycardia, nausea,

vomiting.

Fig. Overview of Patient Enrollment and Hemodynamic Support.

N Engl J Med, Vol. 345, No. 19November 8,

Fig. Protocol for Early Goal-Directed Therapy.

N Engl J Med, Vol. 345, No. 19November 8,

Be a Good Student with Active Learning and Share

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Think Globally but Act Locally
(WHO Statement)

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