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Classification of Shock
Hypovolemic
Cardiogenic
Obstructive
Distributive
Pathophysiology
Preload
Afterload
Contractility
O2 Content
x
O2 Delivery
Cardiac
Output
Resistance
x
Arterial Blood
Pressure
Pathophysiology
BP = CO x R
CO = SV x HR
SV components = Preload, Afterload,
Contractility
DO2 = CO x CaO2
CaO2= (Hb x sat x 1.34) + (PaO2 x 0.003)
Pathophysiology
Shock
CO
Hipovolemik
(preload dan
(termasuk perdarahan) afterload)
Kardiogenik
(kontraktilitas)
Distributif
(termasuk anafilaktik,
septik, neurogenik/
spinal)
sebagai
kompensasi
SVR
sebagai
kompensasi
sebagai
kompensasi
Characteristics of Shock
End organ
dysfunction:
Metabolic
dysfunction:
reduced urine
output
acidosis
altered mental
status
poor peripheral
perfusion
altered metabolic
demands
Therapy
Goal :
pengangkutan O2 &
kebutuhan O2
Keterangan: angka normal analisis gas darah (arteri): pH: 7,35-7,45 ; PCO2: 35-45 mmHg ; HCO3: 22-26 mmol/L.
pH
PCO2
Alkalosis respiratorik
Asidosis metabolik
jika
terkompensasi
Alkalosis metabolik
jika
terkompensasi
HCO3
Penyebab umum
jika
terkompensasi
jika
terkompensasi
Hiperventilasi,
sepsis
Dehidrasi berat,
DM, gagal ginjal,
starving
Muntah
HYPOVOLEMIC SHOCK
Kelas II
Kelas III
Kelas IV
750-1500
1500-2000
>2000
15-30%
30-40%
>40%
Nadi
<100
>100
>120
>140
Tekanan darah
Normal
Normal
Menurun
Menurun
Tekanan nadi
Menurun
Menurun
Menurun
Frekuensi nafas
14-20
20-30
30-40
>35
Produksi urin
(ml/jam)
Status mental
>30
20-30
5-15
Tidak berarti
Sedikit cemas
Agak cemas
Cemas, bingung
Bingung, letargis
Penggantian
cairan
Kristaloid
Kristaloid
Kristaloid dan
darah
Kristaloid dan
darah
Therapy - Hypovolemic
PRINSIP TERAPI : CAIRAN
TUJUAN
VOL. INTRAVASKULER TERCUKUPI
KOREKSI ASIDOSIS METABOLIK
OBATI PENYEBAB
IV fluids
Crystalloid solutions (isotonic)
Both 0.9% saline and RL are equally effective
RL may be preferred in hemorrhagic shock because it
somewhat minimizes acidosis and will not cause
hyperchloremia.
For patients with acute brain injury, 0.9% saline is preferred.
CARDIOGENIC SHOCK
Therapy - Cardiogenic
Terapi Inisial Dg. Pemberian Cairan
Bila Tak Ada Perbaikan
Syok Kardiogenik
memburuk
Inotropik
susp.
zdvnk
DISTRIBUTIVE SHOCK
Distributive Shock
Inflammatory mediators disruption of cellular
metabolism peripheral vasodilation
decreased PVR
Etiology
Anaphylaxis
Septic
Neurogenic
Anaphylactic Shock
Anaphylactic shock
a type of distributive shock, which involves the immune system
(Hurst, 2008)
Type 1 hypersensitivity
antigen binds to IgE antibodies on mast cells, which leads to
degranulation of the mast cells
Management
Anaphylactic Shock
1.
2.
3.
4.
Administer oxygen.
Maintain an adequate airway.
Remove the allergen that caused the reaction.
Administer epinephrine (0.3 to 0.5 mL of a 1:1.000 solution
IM/SC or 0.3 to 0.5 mL of a 1:10.000 solution IV).
5. Initiale fluid therapy early with normal saline to maintain an
6. Administer vasopressor agents if crystalloid therapy is
inadequate for maintaining CO.
7. Consider other pharmacologic treatments: antihistamines,
bronchodilators, and corticosteroids are other options.
8. Perform cardiac monitoring.
9. Observe for a possible second-phase reaction.
Epinephrine in Anaphylactic
Neurogenic Shock
Neurogenic shock is the rarest form of shock.
Septic Shock Tx
O2
Antibiotics
Fluids
Vasopressor
Indication: persistent hypotension* once
adequate intravascular volume expansion has
been achieved
DOC: NOREPINEPHRINE
*systolic blood pressure <90 mmHg or MAP<65 mmHg
OBSTRUCTIVE SHOCK
Obstructive Shock
CO akibat OBSTRUKSI FISIK terhadap ALIRAN DARAH
PENYEBAB :
TAMPONADE PERIKARD
TENSION PNEUMOTHORAX
CRITICAL COARCTASIO AORTA
STENOSIS AORTA
TERAPI
CAIRAN
ATASI PENYEBAB
Patient Assesment
Level of consciousness
Spontaneous effort vs apneu
Airway and cervical spine injury
Chest expansion
Sign of airway obstruction
Signs of respiratorry distress
Protective airway reflexes
START
Simple Triage and Rapid Treatment
TRIASE
proses pemilihan pasien berdasarkan beratnya kondisi
pasien
RPM
respirasi, perfusi, mental
- Semua proses evaluasi
dalam START harus
dilakukan dalam waktu
kurang dari 60 detik.
Brain Death
Snoring
Crowing
Inspiratory stridor
Expiratory wheeze
Locked Jaw
Locked Jaw
Barton bandage
Bronchus Primarius
CO Poisoning
Cyanide Poisoning
Sources
Naturally in foods (some fruits, lima beans, SINGKONG)
Cyanide salts used in industry
Produced in smoke of burning plastics/synthetics, electroplating,
metal polishing
Mechanism
Inhibits cellular respiration
Tissue cannot utilize O2
Characteristics
Smells
CNS
Dyspnea
Tachypnea
Pulmonary edema
Apnea
Pulmonary
Hypertension,
bradycardia
Hypotension, later in
course
Cardiovascular
collapse
Cardiovascular
Nausea, vomiting
Caustic effects
Gastrointestinal
Cyanide Diagnosis
Clinical picture : sweet almond breath
Lactic acidosis
ABG:
metabolic acidosis
ABG sample
Treatment
Remove from source
Oxygen
Cyanide antidote kit:
Amyl nitrite perle until IV established
Sodium Nitrite (300mg IV)
Peds: 0.33 ml/kg of 10% solution)
Organophosphate Poisoning
Sources
Insecticides, herbicides
Mechanism
Inhibit acethylcholinesterase
ACh accumulates throughout the nervous system
Overstimulation of muscarinic and nicotinic receptors
Characteristics
SLUD + GEM
Organophosphate Poisoning
+ GEM
G : Gastrointestinal
E : Emesis
M : Miosis
Atropine
Competitive inhibitor at autonomic postganglionic cholinergic receptors (GI &
pulmonary smooth muscle, exocrine glands, heart, and eye)
Dosis awal dewasa: 2 mg IM. Dosis dapat digandakan setiap 10 menit
sampai teratropinisasi.
Opiates Intoxication
NALOXONE
Dosage
Adult: As hydrochloride: 0.4-2 mg repeated if necessary at 2-3 min intervals. If there is no
response after a total of 10 mg has been given, consider the possibility of overdosage with
other drugs. Reduce dose for opioid-dependent patients: 0.1-0.2 mg. IM/SC routes may be
used (at IV doses) if IV admin is not feasible.
Child: As hydrochloride: Initially 10 mcg/kg IV followed by 100 mcg/kg IV if necessary.
Alternatively, 0.4-0.8 mg IM or SC, repeated as necessary, if IV admin is not feasible.
Parenteral
Amphetamine Intoxication
Arsenic Toxicity
Methanol Toxicity
Methanol
wood alcohol
organic solvent that, because of its toxicity, can
cause metabolic acidosis, neurologic sequelae,
and even death, when ingested
Complication
Visual loss (optic nerve damage)
Metabolic acidosis
Movement disorder (damage in putamen >>)
Therapy
Therapy
Hemodialysis can easily remove methanol and
formic acid.
Mercury Poisoning
Sensory disturbance
peripheral neuropathy
burning
paresthesia, itching,
Tremor
Gingivitis
Acrodynia
Neuropsychiatric
emotional lability or subtle performance
decline
Death
Mercury Poisoning
Botulinum Toxin