Download - Shock Anestesia
ShockPryambodho, dr.SpAn
Dep.Anestesiologi FKUI/RSCM
Jumat 15 April 2011
What is Shock?
= hypotension ?= low blood pressure ?
= haemorrhage ?= unconscious ?
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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
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Physiological response to shock
• Normally the body can compensate for some decreased tissue perfusion through a variety of mechanisms
• When compensation fails, shock develops and if uncorrected becomes irreversible
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Physiological response to shock
• Sympathetic Nervous System – Adrenal response (neuro-humoral)
• Systemic response–Progressive vasoconstriction–Increased blood flow to major organs–Increased cardiac output–Increased respiratory rate and volume–Decreased urine output (water retention)–Decreased gastric activity
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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
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Shock at the cellular level
• Decreased blood flow to the tissues causes cellular hypoxia
• Anaerobic metabolism begins • Cell swelling, mitochondrial disruption, and
eventual cell death; tissues die; organs fail; organ systems fail
• If Low Perfusion States persists compensatory response fail
Irreversible Death imminent!!
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Normal Hemodynamic
Cardiac OutputVenous Return
Perfusion
A V
VR equals COCO = Heart Rate x Stroke VolumeSV = f . EDV. C. TPR
VR CO
4800 = 60 x 80 cc
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Reaksi kompensasi
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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
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CO = HR x
Preload Contractility Afterload
SV
Rate(f)
Pump(contractility)
Volume(preload)
SVR (afterload)
CO
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Common features of shock
Shock
Heart rate Blood pressure Pulse pressure Arterial pH
Respiratory rate
Peripheral perfusion- cold, pale , clammy
Mentation change
Urine output - Neonate < 2 ml/kg/hour- Infant < 1,5 ml- Pre school age < 1 ml- Adult < 0,5 ml
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Shock Categories
1. Hypovolemic : haemorrarghic, dehydration
– Blood volume problem
2. Cardiogenic : AMI, severe dysrhytmia, pericardial tamponade
– Blood pump and/or rate problem
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Shock Categories
3. Distributive: septic shock, anaphylaxis, neurogenic shock
– Blood vessel problem
4. Obstructive: aortic stenosis, massive pulmonary embolus
– Blood flow problem
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Rapid formulation of working Dx
Defining features of shock• Heart rate • Respiratory rate • Mentation changes• Blood pressure • Urine output • Arterial pH
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Rapid formulation of working Dx
• Defining features in compensatory shock• Can be difficult to detect with subtle indicators
–Tachycardia–Decreased skin perfusion–Alterations in mental status
• Some condition such as medications, age, pregnancy can hide signs and symptoms
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Rapid formulation of working DxIs cardiac output reduced?
High-output hypotension(CO )
Septic shock
Low-cardiac-output(CO )
Cardiogenic & Hypovolemic
Is CO reduced?Pulse pressureDiastolic pressurePeripheral perfusionCapillary refill timeHeart soundsTemperatureWhite cell countSite of infection
No
WarmRapidCrisp or or
++
Yes
CoolSlow
Muffled
-
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Rapid formulation of working DxIs the heart too full?
Reduced pump functionCardiogenic shock
Reduced venous returnHypovolemic shock
Is the heart too full?Symptoms clinical context
Jugular venous pressureS3, S4, gallop rhythmRespiratory crepitationsChest radiograph
YesAngina, ECG
++++++
Large heart Upper lobe flowPulmonary edema
NoHemorrhage, diarrhea,
burns
--
Normal (small)
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Rapid formulation of working DxWhat does not fit?Overlapping etiologies (septic-cardiogenic, septic-hypovolemic, cardiogenic-hypovolemic)Other etiologiesHigh output hypotension
High right atrial pressure hypotension
Nonresponsive hypovolemia
Liver failureSevere pancreatitisTrauma + SIRSThyroid stormArteriovenous fistula
Pulmonary hypotensionRight ventricular infarctionCardiac tamponade
Adrenal insufficiencyAnaphylaxisNeurogenic shock
Get more informationEchocardiography, CVP, Swan-ganz catheterization, etc
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Shock management• Recognize inadequate organ perfusion• Identify the cause (working diagnosis)
–Hypovolemic–Cardiogenic–Distributive–Obstructive
• Restore the organ perfusion and tissue oxygenation–Oxygen and ventilatory support–Fluid therapy–Inotrope or vasoactive drugs–Treat the cause
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Shock management• Recognize inadequate organ perfusion• Identify the cause (working diagnosis)
–Hypovolemic–Cardiogenic–Distributive–Obstructive
• Restore the organ perfusion and tissue oxygenation–Oxygen and ventilatory support–Fluid therapy–Inotrope or vasoactive drugs–Treat the cause
ABC resusitasi
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Goals of Respiratory Management
• To protect the airway• To correct inadequate oxygenation and
ventilation• To rest the respiratory muscle
• Caution in cervical trauma!
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Goals Therapy of Shock
• Reverse the pathophysiologic abnormalities• Avoid adverse consequences of excessive
therapy• Titration: “too little vs too much”• Test Response
• Maintain body temperature!
C-EJumat 15 April 2011
Shock management
Volume expansion InotropeVasoactive drugs
Heartfull
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Shock management
Volume expansion InotropeVasoactive drugs
Heartfull
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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
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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
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Fluid management in traumatic/haemorrargic shock
Shock
Fluid Loading 1000-2000 ml
Good response
MildBlood loss
Transient response
Maintenance
Moderate lossOn going losses
Fluid/blood
No response
SevereBlood loss
ShockNon-hypovolemic
Fluid/blood Re-evaluate
Surgicalconsultation
Surgicalconsultation
Surgicalresuscitation
Warm fluid!!
Get moreinformation
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Re-assess Organ PerfusionMonitor• Vital signs• CNS state• Peripheral perfusion• Pulse oximetry• Urine output
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Vasoactive & Inotropic agents• Use after fluid resuscitation failed (normovolemia)
–More efficacious if normovolemia–May obscure hypovolemia
70 100 mmHg
• epinephrine• norepinephrine• dopamin • dopamin (shock)
• norepinephrine (+dopamin)• dobutamin (shock -)
• nitroglycerin (ischemia)• nitropruside
systolic
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Vasoactive & Inotropic agents
• After fluid resuscitation !!• Elevate MAP to 60-65 mmHg• Watch out: Excessive vasoconstriction
monitor lactate!–Ischemia–Contractility
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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
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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
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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
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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.
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Anaphylactic shockSubsequent management
• Give an(histamines ( chlorpheniramine 10‐20 mg slowly IV )
• Give cor(costeroids (200mg hydrocor(sone IV )
• Bronchodilators ( salbutamol 250ugIV or 2.5‐5mg by nebulizer, aminophylline 250mg up to 5mg/kg by slow IV)
• Refer to ICU
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Old and New Paradigm of Shock
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Old and New Paradigm of Shock
Shock
Ischemic Cellular Damage
Organ Failure
Death
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Old and New Paradigm of Shock
Shock
Ischemic Cellular Damage
Organ Failure
Death
Shock
Hypoxic Cellular Priming
Cellular Damage
Multiple Organ Failure
Death
Reperfusion Injury Inflammation
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Hemorrhage
Cellular ischemia
Reperfusion injury
VasoconstrictionMicrocirculatory thrombosis
Leukocyte/platelet/RBC aggregation
Microcirculatory flow maldistribution
Leukocyte-mediated cell injuryCytokine and other mediator
effects, locally and systemically
Gut translocationSepsis
Trauma Hypoxia
Prime insult
Resuscitation
Primary perpetuators
Secondary perpetuators
Tertiary perpetuators
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Haldane
Hypoxia not only stops the machine It wrecks the machine!
Time saving is life saving!
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Haldane
Hypoxia not only stops the machine It wrecks the machine!
Time saving is life saving!
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Summary• Early recognition of shock state• Oxygenation and ventilation• Restore organ perfusion• Monitor patient response• Titrate therapy• Prompt and appropriate action
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Thank U 4 your attention!
Jumat 15 April 2011
Thank U 4 your attention!
Jumat 15 April 2011