Shock

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Shock Shock Nasman Puar, dr.SpAn Bagian Anestesiologi Fakultas Kedokteran Unand/ RSUP Dr. M. Djamil Padang

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Shock. Nasman Puar, dr.SpAn Bagian Anestesiologi Fakultas Kedokteran Unand/ RSUP Dr. M. Djamil Padang. What is Shock?. = hypotension ? = low blood pressure ? = haemorrhage ? = unconscious ?. Shock =. Clinical syndrome - PowerPoint PPT Presentation

Transcript of Shock

Page 1: Shock

ShockShockShockShock

Nasman Puar, dr.SpAn

Bagian Anestesiologi

Fakultas Kedokteran Unand/

RSUP Dr. M. Djamil Padang

Page 2: Shock

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 xCO = HR x

PreloadPreload ContractilityContractility AfterloadAfterload

SVSV

RateRate(f)(f)

PumpPump(contractility)(contractility)

VolumeVolume(preload)(preload)

SVR (afterload)SVR (afterload)

COCO

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Common features of shock

ShockShock

Heart rate Heart rate Blood pressure Blood pressure Pulse pressure Pulse pressure Arterial pH Arterial pH

Respiratory rate Respiratory rate

Peripheral perfusionPeripheral perfusion- cold, pale , clammy- cold, pale , clammy

Mentation changeMentation change

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

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Shock Categories

1.1. Hypovolemic :Hypovolemic : haemorrarghic, dehydration

– Blood volume problem

2.2. Cardiogenic :Cardiogenic : AMI, severe dysrhytmia, pericardial tamponade

– Blood pump and/or rate problem

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Shock Categories

3.3. Distributive:Distributive: septic shock, anaphylaxis, neurogenic shock

– Blood vessel problem

4.4. Obstructive:Obstructive: aortic stenosis, massive pulmonary embolus

– Blood flow problem

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Rapid formulation of working Dx

Defining features of shockDefining 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 shockDefining 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?Is 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?Is 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?What does not fit?Overlapping etiologies (septic-cardiogenic, septic-Overlapping etiologies (septic-cardiogenic, septic-hypovolemic, cardiogenic-hypovolemic)hypovolemic, cardiogenic-hypovolemic)Other etiologiesOther etiologies

High 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

ABC ABC resusitasiresusitasi

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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 - BA - 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-EC-E

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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 shockFluid deficit may exist in all kinds of shock• Is the heart too full?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 Fluid management in traumatic/haemorrargic shocktraumatic/haemorrargic shock

ShockShock

Fluid Loading 1000-2000 mlFluid Loading 1000-2000 ml

Good responseGood response

MildMildBlood lossBlood loss

Transient responseTransient response

MaintenanceMaintenance

Moderate lossModerate lossOn going lossesOn going losses

Fluid/bloodFluid/blood

No responseNo response

SevereSevereBlood lossBlood loss

ShockShockNon-hypovolemicNon-hypovolemic

Fluid/bloodFluid/blood Re-evaluateRe-evaluate

SurgicalSurgicalconsultationconsultation

SurgicalSurgicalconsultationconsultation

SurgicalSurgicalresuscitationresuscitation

Warm fluid!!Warm fluid!!

Get moreGet moreinformationinformation

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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

7070 100100 mmHgmmHg

• epinephrineepinephrine• norepinephrinenorepinephrine• dopamindopamin • dopamin (shock)dopamin (shock)

• norepinephrine (+dopamin)norepinephrine (+dopamin)• dobutamin (shock -)dobutamin (shock -)

• nitroglycerin (ischemia)nitroglycerin (ischemia)• nitroprusidenitropruside

systolicsystolic

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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 hypotensionmay be repeated after 10 - 20 mnt.

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Anaphylactic shock

Subsequent management• Give antihistamines ( chlorpheniramine 10-20 mg

slowly IV ) • Give corticosteroids (200mg hydrocortisone 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 ShockShock

Ischemic Cellular Damage

Organ Failure

Death

Shock

Hypoxic Cellular Priming

Cellular Damage

Multiple Organ Failure

Death

Reperfusion Injury Inflammation

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HemorrhageHemorrhage

Cellular ischemiaCellular ischemia

Reperfusion injuryReperfusion injury

VasoconstrictionVasoconstrictionMicrocirculatory thrombosisMicrocirculatory thrombosis

Leukocyte/platelet/RBC aggregationLeukocyte/platelet/RBC aggregation

Microcirculatory flow maldistributionMicrocirculatory flow maldistribution

Leukocyte-mediated cell injuryLeukocyte-mediated cell injuryCytokine and other mediatorCytokine and other mediator

effects, locally and systemicallyeffects, locally and systemically

Gut translocationGut translocationSepsisSepsis

TraumaTrauma HypoxiaHypoxia

Prime insultPrime insult

ResuscitationResuscitation

Primary perpetuatorsPrimary perpetuators

Secondary perpetuatorsSecondary perpetuators

Tertiary perpetuatorsTertiary perpetuators

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HaldaneHaldane

Hypoxia not only stops the machine It wrecks the machine! 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!