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What is Shock?
= hypotension ? = low blood pressure ? = haemorrhage ? = unconscious ?
Shock =
Clinical syndrome Associated with signs of hypoperfusion: mental status change, oliguria, acidosis, etc May be associated with hypotension Inadequate organ perfusion and tissue oxygenation to meet tissue oxygen demand
Pathophysiology
Initially, neurohumoral compensatory mechanisms maintain perfusion to vital organs If appropriate treatment is not promptly instituted, these compensatory mechanisms are overwhelmed, producing ischemia, cellular damage, multiple organ failure and death
Normal Hemodynamic
Venous Return VR
Cardiac Output CO
4800 = 60 x 80 cc
Perfusion
Reaksi kompensasi
Pathophysiology
Imbalance between organ perfusion & oxygen demand DO2 = Oxygen content x Cardiac output Oxygen content depends on Hb & SaO2 SaO2 depends on Airway & Breathing Cardiac Output & Hb are parts of Circulation matters
Volume (preload)
CO
CO = HR x SV
Preload
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Contractility
Afterload
Shock
Respiratory rate
Urine output - Neonate < 2 ml/kg/hour - Infant < 1,5 ml - Pre school age < 1 ml - Adult < 0,5 ml
Shock Categories
1. Hypovolemic : haemorrarghic, dehydration
Blood volume problem
Shock Categories
3. Distributive: septic shock, anaphylaxis, neurogenic shock
Blood vessel problem
Shock management
Recognize inadequate organ perfusion Identify the cause (working diagnosis)
Hypovolemic Cardiogenic Distributive Obstructive
Shock management
Recognize inadequate organ perfusion Identify the cause (working diagnosis)
Hypovolemic Cardiogenic Distributive Obstructive
A-B
C-E
Shock management
Volume expansion
Heart full
Shock management
Volume expansion
Heart full
Fluid challenge
Fluid deficit may exist in all kinds of shock Is the heart too full?
No : Crystalloid 1 2 L (20 ml/kg) fast Not too full (cardiogenic shock without obvious fluid overload) Crystalloid 250 ml in 20 minute Yes : No fluid challenge
Fluid challenge
Assess patient response Next therapeutic decision depend on patient response
Better : continue with fluid challenge Transient :
Continue with fluid therapy On going losses : find and fix
No response:
Severe hypovolemia
Other etiologies
systolic
70
100
mmHg
epinephrine nitroglycerin (ischemia) norepinephrine nitropruside dopamin dopamin (shock) norepinephrine (+dopamin) dobutamin (shock -)
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Anaphylactic shock
Severe systemic hypersensitivity reaction Characterized by: hypotension & airway compromise Potentially life threatening Classic tipe I hypersensitivity reaction (mediated by IgE) Watch out: mild allergic reaction may progress to severe anaphylaxis
Anaphylactic shock
Inadequate perfusion of tissues through maldistribution of blood flow Intravascular volume is maldistributed because of alterations in blood vessels Cardiac pump & blood volume are normal but blood is not reaching the tissues
Anaphylactic shock
History & physical examination Clinical signs of systemic allergic: urticaria, angioedema, abdominal pain, nausea & vomiting, bronchospasm, rhinorrhea, cutaneus flushing, etc + Hypotension & airway compromise !! Begin: within first hour - 8 hours after exposure The faster onset, the more severe
Anaphylactic shock
Therapy: ABC resuscitation first !!! Drug: Epinephrine
adult: 0,3 - 0,5 mg SC or IM (1:1000) 0,1 mg IV (1:100.000) children: 0,01mg/kg SC or IM (1:1000)
only given after ABC resusitasion, no cardiac arrest, in severe hypotension may be repeated after 10 - 20 mnt.
Anaphylactic shock
Subsequentmanagement Givean(histamines(chlorpheniramine1020mgslowly IV) Givecor(costeroids(200mghydrocor(soneIV) Bronchodilators(salbutamol250ugIVor2.55mgby nebulizer,aminophylline250mgupto5mg/kgbyslow IV) RefertoICU
Organ Failure
Death
Inflammation
Trauma
Hemorrhage
Primary perpetuators
Leukocyte-mediated cell injury Cytokine and other mediator effects, locally and systemically
Secondary perpetuators
Tertiary perpetuators
Haldane
Haldane
Summary
Early recognition of shock state Oxygenation and ventilation Restore organ perfusion Monitor patient response Titrate therapy Prompt and appropriate action