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

Jumat 15 April 2011

Old and New Paradigm of Shock

Shock

Ischemic Cellular Damage

Organ Failure

Death

Jumat 15 April 2011

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!

Jumat 15 April 2011

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

Jumat 15 April 2011

Thank U 4 your attention!

Jumat 15 April 2011

Thank U 4 your attention!

Jumat 15 April 2011