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Shock Definition

A physiological state characterized by a


significant, systemic reduction in tissue
perfusion, resulting in decreased tissue
oxygen delivery and insufficient removal of
cellular metabolic products, resulting in
tissue injury.

Classification of Shock

Hypovolemic

Cardiogenic

Obstructive

Distributive

Pathophysiology
Preload
Afterload
Contractility

Stroke Volume x Heart Rate

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

Cara : O2, cairan, kontrol suhu, antibiotik, koreksi kelainan


metabolik, Inotropik
Airway : intubasi & kontrol ventilasi
Breathing :
Awal : O2 100 %, monitor saturasi
Sirkulasi
Akses IV scr cepat.
Intra osseus: anak 4 6 th
Kateter vena sentral

Acid Base Regulation

Keterangan: angka normal analisis gas darah (arteri): pH: 7,35-7,45 ; PCO2: 35-45 mmHg ; HCO3: 22-26 mmol/L.

Gangguan Asam Basa


Gangguan asam
basa
Asidosis respiratorik

pH

PCO2

Alkalosis respiratorik
Asidosis metabolik

jika
terkompensasi

Alkalosis metabolik

jika
terkompensasi

HCO3

Penyebab umum

jika
terkompensasi

PPOK, asma, ARDS

jika
terkompensasi

Hiperventilasi,
sepsis
Dehidrasi berat,
DM, gagal ginjal,
starving
Muntah

HYPOVOLEMIC SHOCK

Perkiraan Kehilangan Darah


Kelas I

Kelas II

Kelas III

Kelas IV

Kehilangan darah <750


(mL)*
Kehilangan darah <15%
(% volume darah)

750-1500

1500-2000

>2000

15-30%

30-40%

>40%

Nadi

<100

>100

>120

>140

Tekanan darah

Normal

Normal

Menurun

Menurun

Tekanan nadi

Normal atau naik

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

*) untuk laki-laki dengan berat badan 70kg

Therapy - Hypovolemic
PRINSIP TERAPI : CAIRAN
TUJUAN
VOL. INTRAVASKULER TERCUKUPI
KOREKSI ASIDOSIS METABOLIK
OBATI PENYEBAB

REASSES PERFUSI, UO, TANDA VITAL


PILIHAN :
KRISTALOID ISOTONIK : 20 CC/KG SCR CEPAT BILA FUNGSI
JANTUNG NORMAL
NS DAPAT MENYEBABKAN ASIDOSIS HIPERCHLOREMIK

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.

Colloid solutions (eg, HES, albumin, dextrans)


also effective for volume replacement during major
hemorrhage.
offer NO major advantage over crystalloid solutions, and
albumin has been associated with poorer outcomes in patients
with traumatic brain injury.
Sumber: Merck Manuals

End point and Monitoring


The actual end point of fluid therapy in shock is normalization
of DO2
Adequate end-organ perfusion is best indicated by urine
output of > 0.5 to 1 mL/kg/h
Central Venous Pressure
is the pressure in the superior vena cava, reflecting right ventricular enddiastolic pressure or preload.
Normal CVP: 2 to 7 mm Hg (3 to 9 cm H2O)
CVP > 12 to 15 mm Hg : fluid administration risks fluid overload

CARDIOGENIC SHOCK

Therapy - Cardiogenic
Terapi Inisial Dg. Pemberian Cairan
Bila Tak Ada Perbaikan
Syok Kardiogenik

memburuk

Inotropik

susp.

zdvnk

Anaphylactic Septic Neurogenic

DISTRIBUTIVE SHOCK

Distributive Shock
Inflammatory mediators disruption of cellular
metabolism peripheral vasodilation
decreased PVR
Etiology
Anaphylaxis
Septic
Neurogenic

Sign & symptoms


Febrile, tachycardia, clear lungs *, warm extremities,
flat neck veins, oliguria

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

Sign & symptoms


itching, hives, and swelling
circulatory collapse (vasodilatation)
suffocation (bronchial and tracheal swelling)

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.

It is caused by trauma to the spinal cord sudden loss


of autonomic and motor reflexes below the injury level
Stimulation by sympathetic nervous system (-) the vessel
walls relax uncontrollably sudden decrease in peripheral
vascular resistance vasodilation and hypotension

Gambar 4. Patofisiologi spinal 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

Opening the Airway Triple Airway


Maneuver
Slightly extend neck
(when cervival spine
injury not suspected)
Elevated mandible
Open mouth

Hand Positioning the Triple Airway


Maneuver

Oro Pharyngeal Airway

Reassess Spontaneous Breathing


(Ventilation) when Airway Open
Adequate
Oxygen
supplementation
Inadequate
Manual assisted
ventilation

START
Simple Triage and Rapid Treatment

TRIASE
proses pemilihan pasien berdasarkan beratnya kondisi
pasien

Terdiri dari 4 prioritas penanganan:


Merah immediate care/life-threatening
Kuning urgent care/can delay up to 1 hour
Hijau delayed care/can delay up to 3 hours
Hitam dead/no care required

RPM
respirasi, perfusi, mental
- Semua proses evaluasi
dalam START harus
dilakukan dalam waktu
kurang dari 60 detik.

Brain Death

Recognition of Airway Obstruction


Systematic method of detecting airway
obstruction :
Look, listen and feel
Look for chest and abdominal movement
Listen and feel for airflow at the mouth and nose.

Recognition of Airway Obstruction


Gurgling

liquid or semisolid foreign material in the main


airway.

Snoring

pharyng is partially occluded by soft palate or


epiglottis.

Crowing

sound of laryngeal spasm.

Inspiratory stridor

obsruction at laryngeal level or above.

Expiratory wheeze

obstruction of the lower airway.

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

Cyanide inhibit cellular respiration

Clinical Effects of Cyanide


Headache
Dizziness
Seizures
Coma

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)

Sodium Thiosulfate (12.5gm IV)


Peds: 1.65 ml/kg of 25% solution

Djengkolic Acid Poisoning


Sources
JENGKOL bean
Mechanism
poor solubility under acidic conditions
the amino acid precipitates into crystals
mechanical irritation of the renal tubules and urinary tract
Characteristics
abdominal discomfort, loin pains, severe colic, nausea,
vomiting, dysuria, gross hematuria, and oliguria, occurring 2 to
6 hours after the beans were ingested.

Djengkolic Acid Poisoning


Supporting examination
Urine analysis erythrocytes, epithelial
cells, protein, and the needle-like crystals of
djenkolic acid.
Treatment
Hydration to increase urine flow
Alkalinization of urine by sodium
bicarbonate.

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

Sign and Symptom

+ 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.

The main concern with OP toxicity is respiratory failure from


excessive airway secretions. The endpoint for atropinization
is dried pulmonary secretions and adequate oxygenation.
Tachycardia and mydriasis must not be used to limit or to stop
subsequent doses of atropine.

Opiates Intoxication

Antidote for Opiate 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,

Visual field constriction


Ataxia
Cognitive decline
Bizarre behavior
excessive shyness or aggression

Tremor
Gingivitis
Acrodynia
Neuropsychiatric
emotional lability or subtle performance
decline

Death

Mercury Poisoning

Congenital Minamata Disease:


CP, MR, seizure

Botulinum Toxin