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. neurogenik/ spinal) sebagai kompensasi SVR sebagai kompensasi sebagai kompensasi . septik.

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Characteristics of Shock End organ dysfunction: Metabolic dysfunction: reduced urine output acidosis altered mental status poor peripheral perfusion altered metabolic demands .

cairan. antibiotik. kontrol suhu. koreksi kelainan metabolik. Intra osseus: anak 4 6 th Kateter vena sentral . monitor saturasi Sirkulasi Akses IV scr cepat. Inotropik Airway : intubasi & kontrol ventilasi Breathing : Awal : O2 100 %.Therapy Goal : pengangkutan O2 & kebutuhan O2 Cara : O2.

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Acid Base Regulation .

asma. starving Muntah . PCO2: 35-45 mmHg . HCO3: 22-26 mmol/L.45 . DM. sepsis Dehidrasi berat. gagal ginjal.35-7.Keterangan: angka normal analisis gas darah (arteri): pH: 7. ARDS jika terkompensasi Hiperventilasi. 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.

HYPOVOLEMIC SHOCK .

letargis Penggantian cairan Kristaloid Kristaloid Kristaloid dan darah Kristaloid dan darah *) untuk laki-laki dengan berat badan 70kg .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.

Hypovolemic PRINSIP TERAPI : CAIRAN TUJUAN VOL. INTRAVASKULER TERCUKUPI KOREKSI ASIDOSIS METABOLIK OBATI PENYEBAB REASSES PERFUSI. TANDA VITAL PILIHAN : KRISTALOID ISOTONIK : 20 CC/KG SCR CEPAT BILA FUNGSI JANTUNG NORMAL NS DAPAT MENYEBABKAN ASIDOSIS HIPERCHLOREMIK . UO.Therapy .

Sumber: Merck Manuals . dextrans) also effective for volume replacement during major hemorrhage.IV fluids Crystalloid solutions (isotonic) Both 0. For patients with acute brain injury. 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. offer NO major advantage over crystalloid solutions. albumin. Colloid solutions (eg. HES. and albumin has been associated with poorer outcomes in patients with traumatic brain injury.9% saline is preferred.

Normal CVP: 2 to 7 mm Hg (3 to 9 cm H2O) CVP > 12 to 15 mm Hg : fluid administration risks fluid overload .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.

CARDIOGENIC SHOCK .

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.Cardiogenic Terapi Inisial Dg. Pemberian Cairan Bila Tak Ada Perbaikan Syok Kardiogenik memburuk Inotropik susp.Therapy .

zdvnk .

Anaphylactic Septic Neurogenic DISTRIBUTIVE SHOCK .

warm extremities. clear lungs *.Distributive Shock Inflammatory mediators disruption of cellular metabolism peripheral vasodilation decreased PVR Etiology Anaphylaxis Septic Neurogenic Sign & symptoms Febrile. tachycardia. flat neck veins. oliguria .

which leads to degranulation of the mast cells Sign & symptoms itching.Anaphylactic Shock Anaphylactic shock a type of distributive shock. 2008) Type 1 hypersensitivity antigen binds to IgE antibodies on mast cells. hives. and swelling circulatory collapse (vasodilatation) suffocation (bronchial and tracheal swelling) . which involves the immune system (Hurst.

Remove the allergen that caused the reaction. bronchodilators.Management Anaphylactic Shock 1.3 to 0. Maintain an adequate airway.000 solution IV). 3. Administer oxygen. 9.5 mL of a 1:10.000 solution IM/SC or 0. Initiale fluid therapy early with normal saline to maintain an 6.5 mL of a 1:1.3 to 0. Administer epinephrine (0. 5. 4. 7. Observe for a possible second-phase reaction. Consider other pharmacologic treatments: antihistamines. 2. Perform cardiac monitoring. Administer vasopressor agents if crystalloid therapy is inadequate for maintaining CO. and corticosteroids are other options. 8. .

Epinephrine in Anaphylactic .

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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 .

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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 .

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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.Semua proses evaluasi dalam START harus dilakukan dalam waktu kurang dari 60 detik. . mental .

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.

Snoring pharyng is partially occluded by soft palate or epiglottis.Recognition of Airway Obstruction Gurgling liquid or semisolid foreign material in the main airway. Inspiratory stridor obsruction at laryngeal level or above. Expiratory wheeze obstruction of the lower airway. Crowing sound of laryngeal spasm. .

Locked Jaw .

Locked Jaw .

Barton bandage .

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Bronchus Primarius .

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CO Poisoning .

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lima beans. metal polishing Mechanism Inhibits cellular respiration Tissue cannot utilize O2 Characteristics Smells . SINGKONG) Cyanide salts used in industry Produced in smoke of burning plastics/synthetics. electroplating.Cyanide Poisoning Sources Naturally in foods (some fruits.

Cyanide inhibit cellular respiration .

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vomiting Caustic effects Gastrointestinal . later in course Cardiovascular collapse Cardiovascular Nausea. bradycardia Hypotension.Clinical Effects of Cyanide Headache Dizziness Seizures Coma CNS Dyspnea Tachypnea Pulmonary edema Apnea Pulmonary Hypertension.

Cyanide Diagnosis Clinical picture : sweet almond breath Lactic acidosis ABG: metabolic acidosis ABG sample .

5gm IV) Peds: 1.65 ml/kg of 25% solution .33 ml/kg of 10% solution) Sodium Thiosulfate (12.Treatment Remove from source Oxygen Cyanide antidote kit: Amyl nitrite perle until IV established Sodium Nitrite (300mg IV) Peds: 0.

gross hematuria. loin pains. dysuria. vomiting. severe colic. nausea. occurring 2 to 6 hours after the beans were ingested.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. and oliguria. .

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

herbicides Mechanism Inhibit acethylcholinesterase ACh accumulates throughout the nervous system Overstimulation of muscarinic and nicotinic receptors Characteristics SLUD + GEM .Organophosphate Poisoning Sources Insecticides.

Organophosphate Poisoning .

Sign and Symptom + GEM G : Gastrointestinal E : Emesis M : Miosis .

Dosis dapat digandakan setiap 10 menit sampai teratropinisasi.Atropine Competitive inhibitor at autonomic postganglionic cholinergic receptors (GI & pulmonary smooth muscle. The main concern with OP toxicity is respiratory failure from excessive airway secretions. . exocrine glands. 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. and eye) Dosis awal dewasa: 2 mg IM. heart.

Opiates Intoxication .

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1-0.8 mg IM or SC. Child: As hydrochloride: Initially 10 mcg/kg IV followed by 100 mcg/kg IV if necessary. repeated as necessary. consider the possibility of overdosage with other drugs. IM/SC routes may be used (at IV doses) if IV admin is not feasible. If there is no response after a total of 10 mg has been given.4-2 mg repeated if necessary at 2-3 min intervals.2 mg.Antidote for Opiate Intoxication: NALOXONE Dosage Adult: As hydrochloride: 0.4-0. Alternatively. Reduce dose for opioid-dependent patients: 0. if IV admin is not feasible. Parenteral . 0.

Amphetamine Intoxication .

Arsenic Toxicity .

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because of its toxicity. when ingested Complication Visual loss (optic nerve damage) Metabolic acidosis Movement disorder (damage in putamen >>) . can cause metabolic acidosis. neurologic sequelae. and even death.Methanol Toxicity Methanol wood alcohol organic solvent that.

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

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Botulinum Toxin .