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Management of Shock

Pembimbing: dr Rory Denny Saputra

Galih Rahman

Failure of delivery oxygen and substrates to meet the metabolic demands of the tissue beds
SUPPLY < DEMAND Oxygen delivery < Oxygen Consumption DO2 < VO2

Failure to remove metabolic end-products Result of inadequate blood flow and/or oxygen delivery

Why should you care?

High mortality - 20-90% Early on the effects of O2 deprivation on the cell are REVERSIBLE Early intervention reduces mortality

Oxygen Transport
Oxygen Transport:
Hemoglobin-bound (97%) Dissolved in plasma (3%)

Hemoglobin-bound (SpO2) Dissolved in plasma (pO2)

Oxygen delivery (DO2)

DO2 = CO x CaO2
DO2 : oxygen delivery CO : Cardiac output CaO2: arterial oxygen content HR: heart rate SV: stroke volume

CO = HR x SV

CaO2 = HgB x SaO2 x 1.34 + (0.003 x PaO2)

Oxygen content = oxygen carried by HgB + dissolved oxygen Normal DO2 is 520 to 570 mL/minute/m2

Oxygen Uptake
VO2 = CO X 1.34 X Hb X (SpO2-SvO2)

O2 supply < O2 demand O2 delivery < O2 consumption DO2 < VO2

Approach to the Patient in Shock

Recent illness Fever Chest pain Abdominal pain Comorbidities Medications Toxins/Ingestions Recent hospitalization or surgery Baseline mental status

Physical examination
Vital Signs CNS mental status Skin color, temp, rashes, sores CV JVD, heart sounds Resp lung sounds, RR, oxygen sat, ABG GI abd pain, rigidity, guarding, rebound Renal urine output

Empiric Criteria for Shock

4 out of 6 criteria have to be met

Ill appearance or altered mental status Heart rate >100 Respiratory rate > 22 (or PaCO2 < 32 mmHg) Urine output < 0.5 ml/kg/hr Arterial hypotension > 20 minutes duration Lactate > 4
- Lactate is increased due to: Decreased O2 --> aerobic metabolism switches over to anaerobic --> byproduct = lactate Decreased hepatic clearance

Goals of Treatment
Airway control work of Breathing optimize Circulation assure adequate oxygen Delivery achieve End points of resuscitation

Airway & Breathing

Decision to intubate and initiate ventilatory support should be made on clinical basis Determine need for intubation but remember: intubation can worsen hypotension
Sedatives can lower blood pressure Positive pressure ventilation decreases preload

Treatment: Airway and Breathing

Consider Intubation Generally no need for intubation
3 reasons to intubate in the setting of shock
Inability to oxygenate Inability to maintain airway Work of breathing
Inability to oxygenate (Pulmonary edema, SaO2 88%) Accessory Muscle Use

Recognize signs of early respiratory failure:

Inability to speak Labored breathing Cyanosis Tachypnea Mental obtundation Paradoxical breathing Diaphoresis Accessory muscle use

Optimizing Circulation
Isotonic crystalloids Titrated to:
CVP 8-12 mm Hg Urine output 0.5 ml/kg/hr (30 ml/hr) Improving heart rate

Maintaining Oxygen Delivery

Decrease oxygen demands
Provide analgesia and anxiolytics to relax muscles and avoid shivering

Maintain arterial oxygen saturation/content

Give supplemental oxygen Maintain Hemoglobin > 10 g/dL

Serial lactate levels or central venous oxygen saturations to assess tissue oxygen extraction

End Points of Resuscitation

Goal of resuscitation is to maximize survival and minimize morbidity Goal directed approach
Urine output > 0.5 mL/kg/hr CVP 8-12 mmHg MAP 65 to 90 mmHg

Shock (Classifications)
Physiological classifications better describe underlying problem:
Hypovolemic Shock Cardiogenic Shock Obstructive Shock Distributive Shock
Spinal Shock Septic Shock Anaphylactic

Hypovolemic Shock

Hypovolemic Shock
Vomiting Diarrhea Bowel obstruction, pancreatitis Burns Neglect, environmental (dehydration) GI bleed Trauma Massive hemoptysis AA rupture Ectopic pregnancy, post-partum bleeding


Hypovolemic Shock
Hemorrhagic shock is caused by a loss of intravascular fluid which is usually whole blood or plasma

Critical Care and Resuscitation 2000; 2: 55-65

Hemorrhagic Shock
Compensated Stage
Mechanism: Volume depletion due to bleeding.
Body detects decrease in cardiac output.

Sympathetic nervous system is stimulated releasing epinephrine and norepinehrine to stimulate alpha and beta receptors.
Alpha = Vasoconstriction

Beta = bronchodilation and cardiac stimulation.


Hemorrhagic (Classic) Shock: Compensated Signs and Symptoms

Mental Status Alert or slight anxiety Skin Blood Pressure Pulse Respiration

Becomes Normal cool, pale. Sweating begins at upper lip and spreads to other areas

Normal to Normal to rapid rapid


Hemorrhagic (Classic) Shock: Progressive

Progressive Stage: Mechanism: Kidneys release anti-diuretic hormone which increases vasoconstriction by closing the capillary sphincters, greatly reducing peripheral circulation. Increased hypo-perfusion causes increase in metabolic acid build up


Hemorrhagic (Classic) Shock: Progressive Signs and Symptoms

Mental Status
Skin Blood Pressure Begins to fall. Capillary refill delayed Pulse Rapid and weak

Respiration Rapid and shallow


Cool , Lethargic, clammy, Pale. sleepy, combative Mottling: Cyanosis around nose and mouth at first, spreads to extremities .

Decreased urination.


Hemorrhagic (Classic) Shock: Irreversible

Mechanism: Compensatory mechanisms fail. Pre-capillary sphincters open releasing metabolic acids, micro-emboli and other wastes into circulation.
Cell damage, organ failure and death occur.


Hemorrhagic (Classic) Shock: Irreversible Signs and Symptoms

Mental status


Blood pressure
Decreases Becomes undetectable




Decreased Grey, LOC, to mottled, unrespon- cyanotic, siveness. waxen. Sweating stops.

Slows then Agonal Irritable disappears. Respiration Heart, BradyCardia, Leads to Asystole .


Grades of Hypovolemic Shock

Sign & symptom Class I Class II 750-1500 15-30 >100 Class III 1500-2000 30-40 >120 Class IV >2000 >40 >140 Blood loss (mL) Up to 750 %Blood volume Up to 15 Pulse rate <100

Blood pressure N Capillary refill


20-30 20-30 Anxiety

30-40 5-15 Confused

>35 Negligible Lethargic


Urinary output >30 (ml/hr) Mental status Fluid replacement Mild anxiety 12L crystalloid, + maintenance

2 L crystalloid, 2 L crystalloid, re-evaluate, re-evaluate replace blood loss 1:3 crystalloid, 1:1 colloid or blood products. Urine output >0.5 mL/kg/hr

Grades of dehydration
Mild < 5% Pulse rate Blood pressure Respiratory rate Capillary return N N N <2 seconds Moderate 5-10% N N 3-4 seconds Severe >10% Rapid >5 seconds

Urine Output
Mucous membran CNS/mental status

Moist N/restless

Dry Drowsy

Parched Lethargic/comatose

5% dehydration = loss of 5 ml of fluid per 100 g body weight or 50 ml per kg


Ringan atau Sedang

Berat atau Syok

Pemberian Cairan Defisit

Dibagi rata dlm 24 jam

Tahap I (rehidrasi cepat) : 20-40 cc/KgBB/1-2 jam Tahap II : sisa defisit 6 jam sisanya 16-17 jam

PERUBAHAN : -Gx Klinis -Hematokrit -Plasma elektrolit -CVP

+ Maintenance

Response to Initial Fluid Resuscitation

Rapid Response Vital Sign Return to Normal Transient Response No Response Transient improvement, recurrent of BP and HR Moderate and ongoing (20%-40%) High Moderate to high Type-specific Likely Remain abnormal

Estimated blood loss Need for more crystalloid Need for blood Blood preparation Need for operative intervention

Minimal (10%-20%) Low Low Type and cross match Possibly

Severe (>40%) High Immediate Emergency blood release Highly likely

Monitoring syok
Monitor terhadap pemberian cairan, meliputi : Perbaikan perfusi (akral hangat, nadi lebih besar, kesadaran membaik dsb) Pantau produksi urin, produksi urin normal : Dewasa : 30-50 cc/jam atau 0.5 cc/KgBB Anak : 1 cc /KgBB Bayi : 2 cc /KgBB

Monitor Respon terhadap pemberian cairan : Bila respon terhadap cairan tidak baik, selalu pertimbangkan kemungkinan syok nonhemoragik Bila respon buruk kemungkinan perdarahan berlanjut, cari sumber perdarahan Cari sumber perdarahan lain : Jika ada therapi stop perdarahan Jika tidak ada berarti non hemoragik, therapi sesuai penyebab

Cardiogenic Shock

Cardiogenic Shock
The heart cannot pump enough blood to meet the metabolic demands of the body.

Cardiogenic Shock : Causes

Decreased Contractility (Myocardial Infarction, myocarditis, cardiomypothy, Post resuscitation syndrome following cardiac arrest) Mechanical Dysfunction (Papillary muscle rupture post-MI, Severe Aortic Stenosis, rupture of ventricular aneurysms etc) Arrhythmia (Heart block, ventricular tachycardia, SVT, atrial fibrillation etc.) Cardiotoxicity (B blocker and Calcium Channel Blocker Overdose)

Pathophysiology of Cardiogenic Shock

Often after ischemia, loss of LV function
Lose 40% of LV clinical shock ensues

CO reduction = lactic acidosis, hypoxia Stroke volume is reduced

Tachycardia develops as compensation Ischemia and infarction worsens

Obstructive Shock

Syok Obstruktif
Disebabkan oleh obstruksi mekanis thd cardiac output dgn penurunan perfusi sistemik Penyebab: a. Cardiac tamponade b. Tension pneumothorax c. Emboli paru masif d. Emboli udara Tanda: distensi vena jugularis, muffled heart sound (tamponade), suara nafas unilateral (pneumothorax) Tx: memaksimalkan preload dan mengatasi obstruksi

Distributive Shock
Sepsis Anaphylactic Neurogenic

Syok distributif
Disebabkan oleh vasodilatasi sistemik krn penyebab yg muncul (infeksi, anafilaksis) hipoperfusi sistemik Syok distributif ditingkatkan oleh respon inflamasi Terjadi hipoksia seluler karena gangguan fungsi mitokondria. Penyebab lain: anaphylaxis, severe trauma, severe liver dysfunction, and neurogenic shock.

Anaphylactic Shock
Shock resulting from widespread hypersensitivity. Form of distributive shock.

Killer Bee

Anaphylactic Shock
Anaphylaxis a severe systemic hypersensitivity reaction characterized by multisystem involvement
IgE mediated

Anaphylactoid reaction clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure
Not IgE mediated

Anaphylactic Shock
Penicillin and related antibiotics Aspirin Trimethoprimsulfamethoxazole (Bactrim, Septra) Vancomycin NSAIDs

Foods and Additives:

Shellfish Soy beans Nuts Wheat Milk Eggs Monosodium glutamate Nitrates and nitrites Tartrazine dyes (food colors)

Hymenoptera stings Insect parts and molds X-Ray contrast media (ionic)

Anaphylactic Shock
What are some symptoms of anaphylaxis?
First- Pruritus, flushing, urticaria appear

Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness Finally- Altered mental status, respiratory distress and circulatory collapse

Kompleks Gejala Anafilaksis

Saluran napas Rinitis Sembab laring


Bendungan nasal & gatal

Edema mukosa Stridor laring Sembab pita suara


Batuk Mengi (Wheezing) Sensasi opresi Retrosternal

Batuk Mengi Ronkhi Gawat napas Takipne

Sistem Kardiovaskular



Hipotensi Takikardia


Perubahan EKG :
ST nonspesifik Perubahan gelombang T, Ritme nodal, Fibrilasi atrial, tak ada nadi

Henti jantung (cardiac arrest)

Perubahan EKG :
Asistol ventrikular Fibrilasi ventrikular


Urtikaria Hives Angioedema Pembengkakan ekstremitas, perioral, periorbital


Lesi Urtikaria tipis


Edema sering asimetris

Sistem gastro intestinal Mata

Nausea, muntah, nyeri perut, diare Konjungtivitish Gatal okular, lakrimasi Inflamasi konjungtival

Terapi Reaksi Anafilaktik dan Anafilaktoid

Jamin jalan napas bebas Lokasikan tempat yang kena racun Pasang ikatan proksimal bila tempat tsb suatu ekstremitas Adrenalin 0,3 0,5 ml lar 1 : 1000 lokal ke dalam tempat tsb Tambahkan oksigen Adrenalin 0,3 0,5 ml lar 1 : 1000 subkutan (ringan) atau intravena (berat) Aminofilin 5 6 mg / kg iv dosis pertama, kemudian : 0,4 0,9 mg/kg jam iv (untuk bronkospasme yang menetap) Pertahankan kadar serum pada 10-20 mcg/kg Cairan (gunakan derajat hemokonsentrasi sebagai penutntun) Pemantauan hemodinamik (tekanan arterial dan pengisian jantung, curah jantung) Cairan Pengobatan inotropik positif menurut variabel hemodinamik Zat vasoaktif Bantuan hidup dasar dan lanjut sesuai metoda dan pengobatan konvensional Henti Jantung Paru (standar ACLS )



Tabel 4 Obat obat yang bermanfaat dalam terapi anafilaksis

Adrenalin alfaagonis

Kerja farmakolog pada anafilaksis

Vasokonstriksi di kulit, mukosa dan splankhnikus

Kerja selular
Meninggikan cAMP

Dosis (dewasa)
0,3 ml 1:1000 IM

Terapi segera dan awal pada semua bentuk anafilaksis


Dilatasi bronkus dan kontriksi arteriole otot Dilatasi bronkus & stimulasi jantung inotropik Meninggikan cAMP 1,0 mg dalam 1000 ml 5% dekstrosa dalam air lewat tetesan IV + Dapat dipakai pada hipotensi normovolemi k (perlu pantauan jantung Hipotensi berat

Isoproterenol betaagonis HCL

Noradrenalin alfaagonis

Dilatasi bronkus & stimulasi jantung inotropik

Menurunkan cAMP

4,0 ml lar 0,2% dalam 1000 ml 5% dekstrosa dalam air lewat tetesan IV

Metaraminol alfaagonis bitartrat

Meninggikan ta-hanan vaskular periferi

100 mg da-lam 1000 ml 5% dekstrosa dalam air le-wat tetesan IV + 25 mg per oral tiap 6 jam


Efedrin alfaagonis sulfat

Sama dengan adrenalin

Reaksi yang berkepanjangan yang memerlukan pemakaian kontinyu betaagonis


Dilatasi bronkus

Meninggikan cAMP

250 mg IV selama 10 menit 50 mg tiap 6 jam IV atau per oral 100 mg tiap 6 jam IV

Bronkospasme yang tak dapat diatasi dengan adrenalin Semua bentuk anafilaksis kecuali bronkospasme yg menetap Bronkospasme yang menetap Hipotensi lama

Difenhidramin HCl

Inhibitor kompetitif histamin pada sel sasaran Tidak diketahui


Tabel 5 : Garis Besar Terapi Anafilaksis

Reaksi Terapi segera Ringan Konyungtivitis Rinitis Urtikaria Pruritus Eritema Sembab laring Adrenalin HCl 0,3 ml 1:1000 SC, IM Difenhidramin HCl 50 mg per oral Adrenalin HCl 0,3 ml 1:1000 IM Difenhidramin HCl 50 mg IV Adrenalin HCl 0,3 ml 1:1000 IM Difenhidramin HCl 50 mg IV Difenhidramin HCl tiap 6 jam Terapi supportif Berat

Difenhidramin HCl 50 mg tiap 6 jam Efedrin sulfat 25 mg tiap 6 jam Adrenalin HCl 0,3 ml 1:1000 IM Aminofilin 250 selama 10 menit

Oksigen Pantau gas darah Trakeostomi Difenhidramin HCl, 50 mg tiap 6 jam Efedrin Sulfat 25 mg tiap 6 jam Hidrokortison Oksigen Pantau gas darah Aminofilin 500 mg IV tiap 6 jam Cairan IV Hidrokortison Awasi terhadap gagal napas Oksigen Metaraminol bitartrat atau noradrenalin IV Pantau EKG Pantau volume darah Cairan IV Isoproterenol HCL dalam hipotensi normovolemik dengan curah jantung rendah Terapi manifestasi primer dengan vasopresor. Terapi aritmia dengan obat antiaritmik O2,





Adrenalin HCl 0,3 ml 1:1000 IM Difenhidramin HCl 50 mg IV

Metaraminol bitartrat 100 mg dalam 1000 ml 5% dekstrosa dalam air


Neurogenic Shock
Interruption in the CNS connections with the periphery (spinal cord injury). Form of distributive shock.

Neurogenic Shock
Occurs after acute spinal cord injury Sympathetic outflow is disrupted leaving unopposed vagal tone Results in hypotension and bradycardia Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)

Neurogenic Shock
Loss of sympathetic tone results in warm and dry skin Shock usually lasts from 1 to 3 weeks Any injury above T1 can disrupt the entire sympathetic system
Higher injuries = worse paralysis

Neurogenic Shock
Loss of sympathetic tone results in warm and dry skin Shock usually lasts from 1 to 3 weeks

Neurogenic Shock- Treatment

Remember c-spine precautions

Fluid resuscitation
Keep MAP at 85-90 mm Hg for first 7 days Thought to minimize secondary cord injury If crystalloid is insufficient use vasopressors

Search for other causes of hypotension For bradycardia

Atropine Pacemaker

Neurogenic Shock- Treatment

Used only for blunt spinal cord injury High dose therapy for 23 hours Must be started within 8 hours Controversial- Risk for infection, GI bleed

Septic Shock
Component of systemic inflammatory response syndrome (SIRS). Form of distributive shock.

Septic Shock

Temp >38 or < 36 Tachycardia (>90x/mnt) Tachypnea (RR > 20) WBC or , bands SIRS Infection (presumed or known) Sepsis Hypotension End organ dysfunction

Septic Shock
Sepsis Hypotension after 40 ml/kg Pressor requirement Further evidence of low perfusion (lactate, oliguria, AMS)


Severe Sepsis


Treatment of Sepsis
Antibiotics- Survival correlates with how quickly the correct drug was given Cover gram positive and gram negative bacteria
Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or Imipenem 1 gram IV

Add additional coverage as indicated

Pseudomonas- Gentamicin or Cefepime MRSA- Vancomycin Intra-abdominal or head/neck anaerobic infections- Clindamycin or Metronidazole Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae Neutropenic Cefepime or Imipenem

Treatment Algorithm

Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med. 2001:345:1368-1377.

To Summarize
Type of Shock Insult Physiologic Effect Compensation


Heart fails to pump blood out


BaroRc SVR
BaroRc SVR BaroRc SVR


Heart pumps well, but CO the outflow is obstructed CO

Hemorrhagic Heart pumps well, but not enough blood volume to pump Distributive Heart pumps well, but there is peripheral vasodilation



The End

Pediatric septic shock