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Shock

Pryambodho, 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
Venous Return VR

Cardiac Output CO

4800 = 60 x 80 cc
Perfusion

VR equals CO CO = Heart Rate x Stroke Volume SV = f . EDV. C. TPR


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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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Volume (preload)

SVR (afterload) Rate (f) Pump (contractility)

CO

CO = HR x SV
Preload
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Contractility

Afterload

Common features of shock


Heart rate Blood pressure Pulse pressure Arterial pH Mentation change

Shock

Respiratory rate

Urine output - Neonate < 2 ml/kg/hour - Infant < 1,5 ml - Pre school age < 1 ml - Adult < 0,5 ml

Peripheral perfusion - cold, pale , clammy

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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 Dx


Is cardiac output reduced?
High-output hypotension (CO ) Septic shock Is CO reduced? Pulse pressure Diastolic pressure Peripheral perfusion Capillary refill time Heart sounds Temperature White cell count Site of infection
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Low-cardiac-output (CO ) Cardiogenic & Hypovolemic Yes Cool Slow Muffled -

No Warm Rapid Crisp or or ++

Rapid formulation of working Dx


Is the heart too full?
Reduced pump function Cardiogenic shock Is the heart too full? Symptoms clinical context Jugular venous pressure S3, S4, gallop rhythm Respiratory crepitations Chest radiograph Yes Angina, ECG +++ +++ Large heart Upper lobe flow Pulmonary edema Reduced venous return Hypovolemic shock No Hemorrhage, diarrhea, burns Normal (small)

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Rapid formulation of working Dx


What does not fit? Overlapping etiologies (septic-cardiogenic, septichypovolemic, cardiogenic-hypovolemic) Other etiologies
High output hypotension Liver failure Severe pancreatitis Trauma + SIRS Thyroid storm Arteriovenous fistula High right atrial pressure hypotension Pulmonary hypotension Right ventricular infarction Cardiac tamponade Nonresponsive hypovolemia Adrenal insufficiency Anaphylaxis Neurogenic shock

Get more information Echocardiography, 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

Jumat 15 April 2011

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!

A-B

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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-E

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Shock management

Volume expansion

Heart full

Inotrope Vasoactive drugs

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Shock management

Volume expansion

Heart full

Inotrope Vasoactive drugs

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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
Warm fluid!!

Good response Mild Blood loss Maintenance


Surgical consultation
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Transient response Moderate loss On going losses Fluid/blood


Surgical consultation

No response Severe Blood loss Fluid/blood


Surgical resuscitation

Shock Non-hypovolemic Re-evaluate


Get more information

Re-assess Organ Perfusion


Monitor 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

systolic

70

100

mmHg

epinephrine nitroglycerin (ischemia) norepinephrine nitropruside dopamin dopamin (shock) norepinephrine (+dopamin) dobutamin (shock -)
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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 shock
Subsequentmanagement Givean(histamines(chlorpheniramine1020mgslowly IV) Givecor(costeroids(200mghydrocor(soneIV) Bronchodilators(salbutamol250ugIVor2.55mgby nebulizer,aminophylline250mgupto5mg/kgbyslow IV) RefertoICU

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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 Shock


Hypoxic Cellular Priming Ischemic Cellular Damage Reperfusion Injury Organ Failure Cellular Damage Death Multiple Organ Failure Death
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Inflammation

Trauma

Hemorrhage

Hypoxia Prime insult

Cellular ischemia Resuscitation Reperfusion injury

Vasoconstriction Microcirculatory thrombosis Leukocyte/platelet/RBC aggregation

Primary perpetuators

Microcirculatory flow maldistribution

Leukocyte-mediated cell injury Cytokine and other mediator effects, locally and systemically

Secondary perpetuators

Gut translocation Sepsis


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Tertiary perpetuators

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