16. Manajemen Shock.ppt

7/27/2019 16. Manajemen Shock.ppt

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Diagnosis and Management

of Shock


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Shock

Always a symptom of primary cause

Inadequate blood flow to meet tissue oxygen

demand May be associated with hypotension

Associated with signs of hypoperfusion: mentalstatus change, oliguria, acidosis


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DEFINISI

IT IS NOTLOW BLOOD PRESSURE!!!

IT ISHYPOPERFUSION..

Gangguan dari perfusi jaringan yang terjadi akibat

adanya ketidakseimbangan antara suplai oksigen kesel dengan kebutuhan oksigen dari sel tersebut.

Semua jenis shock mengakibatkan gangguan padaperfusi jaringan yang selanjutnya berkembang

menjadi gagal sirkulasi akut atau disebut jugasindroma shock


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Shock Categories

Cardiogenic

Hypovolemic

Distributive

Obstructive


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Cardiogenic Shock

Decreased contractility

Increased filling pressures, decreased LV stroke

work, decreased cardiac output Increased systemic

vascular resistance compensatory


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Hypovolemic Shock

Decreased cardiac output

Decreased filling pressures Compensatory increase in

systemic vascular resistance


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Distributive Shock

Normal or increased cardiac output

Low systemic vascular resistance

Low to normal filling pressures Sepsis, anaphylaxis, neurogenic,

and acute adrenal insufficiency


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Obstructive Shock

Decreased cardiac output

Increased systemic vascular resistance

Variable filling pressures dependent

on etiology Cardiac tamponade, tension

pneumothorax, massive pulmonaryembolus


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O2

CARDIOGENIC

HYPOVOLEMIK

O2

O2

OBSTRUCTIVE

SEPTIC


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Cardiogenic Shock Management

Treat arrhythmias

Diastolic dysfunction may require

increased filling pressures

Vasodilators if not hypotensive

Inotrope administration


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Cardiogenic Shock Management

Vasopressor agent needed ifhypotension present to raise aorticdiastolic pressure

Consultation for mechanical assistdevice

Preload and afterload reduction toimprove hypoxemia if blood

pressure adequate


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Hypovolemic Shock

Management

Volume resuscitationcrystalloid, colloid

Initial crystalloid choices

Lactated Ringers solution

Normal saline (high chloride may producehyperchloremic acidosis)

Match fluid given to fluid lost

Blood, crystalloid, colloid


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Distributive Shock Therapy Restore intravascular volume

Hypotension despite volume therapy

Inotropes and/or vasopressors

Vasopressors for MAP < 60 mm Hg

Adjunctive interventions dependent on etiology


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Obstructive Shock Treatment

Relieve obstruction

Pericardiocentesis

Tube thoracostomy

Treat pulmonary embolus Temporary benefit from fluid or

inotrope administration


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Fluid Therapy

Crystalloids

Lactated Ringers solution

Normal saline

Colloids Hetastarch

Albumin

Gelatins

Packed red blood cells Infuse to physiologic endpoints


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Fluid Therapy

Correct hypotension first

Decrease heart rate

Correct hypoperfusion abnormalities Monitor for deterioration of oxygenation


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Inotropic / Vasopressor Agents

Dopamine

Low dose (2-3 g/kg/min)mild inotropeplus renal effect

Intermediate dose (4-10 g/kg/min)inotropic effect

High dose ( >10 g/kg/min)vasoconstriction

Chronotropic effect


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Inotropic Agents

Dobutamine

5-20 g/kg/min

Inotropic and variable chronotropic effects

Decrease in systemic vascular resistance


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Norepinephrine

0.05 g/kg/min and titrate to effect

Inotropic and vasopressor effects

Potent vasopressor at high doses


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Epinephrine

Both and actions for inotropic andvasopressor effects

0.1 g/kg/min and titrate

Increases myocardial O2 consumption


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Therapeutic Goals in Shock

Increase O2 delivery

Optimize O2 content of blood

Improve cardiac output and

blood pressure

Match systemic O2 needs with O2 delivery

Reverse/prevent organ hypoperfusion


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Pediatric Considerations

BP not good indication of hypoperfusion

Capillary refill, extremity temperature bettersigns of poor systemic perfusion

Epinephrine preferable to norepinephrine due to morechronotropic benefit

Fluid boluses of 20 mL/kg titrated to BP or total 60mL/kg, before inotropes or vasopressors


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Pediatric Considerations

Neonatesconsider congenitalobstructive left heart syndrome as cause ofobstructive shock

Oliguria


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How Much Fluid To Give?

Some measure of intravascular filling Pressure (CVP or PAOP)

Some assessment of risk of pulmonary oedema andcapillary leak

Pulmonary gas exchange (PaO2:FiO2) Requirement for positive pressure (PEEP)

Chest X-ray

Some assessment of response to treatment

Changes in acid base balance, lactate Measurement of cardiac output


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What Do You Need to Know When You

Resuscitate a Patient in Shock?

Arterial blood pressure

Urine output

Systemic acidbase balance (pH, SBE, lactate)

Some clinical assessment of tissue perfusion warm and well perfused or cold and shut down

Some measurement of global blood flow and tissue perfusion Cardiac output or cardiac index

Arterial oxygen delivery, oxygen uptake index

Mixed venous saturation and PvO2


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Cardiac Outp ut x SVR

Pipe = VascularPump =

Heart

Volume =

Blood

Hypovolemic

Shock

Cardiogenic

ShockDist r ibut ive

Shock

Inotropes

(Dob,Dop,Adr,Amr)Vasop resso r ( NE,PE,Adr,Dop )

Fluids

Obst ruct ive

Shock

Release

tamponade,etcBlood Pressure


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PATOFISIOLOGI DARI RESPONTUBUH TERHADAP SHOCK

Respon Neuroendokrin

Respon Hemodinamik

Respon Metabolik

FEARN d i R


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HYPOVOLEMIA

R atriumlow-pressure stretch

receptors

Aorta/carotidsHigh-pressurebaroreceptors

LOSS OF TONICINHIBITION OFCENTRAL AND

SYMPATHETICNERVOUS SYSTEMS

RenalRenin release

Pituitary glandACTH, ADH and GH releas

Adrenal gland (medulla)Epinephrine/norepinephrin

release

Adrenal cortexCortisol release

Adrenal cortexAldosterone release

Angiotensin II

Decreased renalperfusion

FEARStimulation of limbic

area of brain

Increased:hypothalamic,

adrenomedullaryadrenocortical activity

Neuroendocrine Respons


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RESPON HEMODINAMIKMekanisme un tuk memperbaik i keseimbangan

kardiovaskular

Redistribusi aliran darah

Peningkatan cardiac output

Memperbaiki volume intravaskular

RESPON HEMODiNAMiK


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STIMULASI NEUROENDOKRIN

HYPOTENSION

BLOOD FLOW PROTECTEDHeart

BrainAdrenal/pituitary gland

BLOOD FLOW DECREASEDSkin

MuscleSplanchnic circulation

RESPON HEMODiNAMiKREDISTRIBUSI ALIRAN DARAH

Limited to 180 beats/minb f d d CO d t


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CARDIAC OUTPUT = HR X SV

Sympathetic n.system

Catecholaminerelease

Increase EDV viaVenoconstr ict ion

Arter iolar con str ict ion

Renal reabsorpt io n

Increasedcontractility

before decreased CO due todecreased diastolic filling

time

Memperbaiki ol me darah


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Memperbaiki volume darah

Transcapillary refill phase1. Decreased capi l lary p ressure caused b y h ypo tension

2. Sympathet ic in crease in precapi l lary arter io lar con str ict ion

Decrease capi l lary hy dros tat ic pressu re promotes passage off lu id from interst i t ium to intravascular space

Plasma protein restitution phaseIncreased plasma osmolar i ty due to m ainly h epat ic release of

gluc ose, pyruvate, amino acids, etc.

Inc reased interst i t ia l osmolarity

Increased interst i t ial volume and pressure

Transc api l lary movement of album in into intravascular space

HAEMODYNAMIC RESPONSES


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HAEMODYNAMIC RESPONSESVenoconstriction

Sympathet ic n. system (SNS)Catecholamines (CA)Ang iotensi n II (ATII)

ADH

Reduced venouscapacitance

Arteriolar constriction

SNS, CA, A TII, ADH

Decreased capillary P

Fluid shift from interstitium intovascular compartment

Increased distal tubularreabsorption

Aldosterone, ADH

Increased proximal tubularreabsorptionSNS, CA, ATII

Increased myocardialcontractility

SNS, CA

Restoration ofblood volume

Increasedventricular

filling P

Increased ventricularejection fraction

SV

CO

BPIncreased heart rateSNS, CA

Increased SVR due toarteriolar construction

SNS, CA, ATII, ADH

SVR


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RESPON METABOLIK

Hyperglikemia

Mobilisasi lemak

Katabolisme/pemecahan ProteinPeningk atan sintesis ur eaPeningk atan asam am ino arom at ik

Penurunan sintesis reactan fase akut

Peningkatan osmolalitas ekstrasel

RESPON METABOLIK


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RESPON METABOLIK

Breakdown ofskeletal muscle

into a.a.

Conversionof a.a. toglucose

Release of:CatecholaminesCortisolGlucagonGrowth hormone

Impairedperipheral

glucose uptake

HYPERGLYCEMIA

Glycogenbreakdown

METABOLIC RESPONS


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METABOLIC RESPONS

Decreased bloodvolume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysisPyruvate converted to lactic acid

METABOLIC ACIDOSIS

METABOLIC RESPONS


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Release of:

CatecholaminesCortisolGlucagon

LIPOLYSIS

INCREASE IN PLASMA FREEFATTY ACIDS

METABOLIC RESPONS

EFEK SHOCK PADA TINGKATAN SEL


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HYPOXIA

LOW-FLOW,

POOR PERFUSION

ANAEROBICMETABOLISM

ACIDOSIS

DECREASED CELLULARENERGY EFFICIENCY

Glucose breakdown (A) Stage one glycolysis is anaerobic (does


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Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does

not require oxygen). It yields pyruvic acid, with toxic by-products

such as lactic acid, and very little energy. (B) Stage two is aerobic

(requires oxygen). In a process called the Krebs or citric acid

cycle, pyruvic acid is degraded into carbon dioxide and water,which produces a much higher yield of energy.



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CELL MEMBRANE FAILURE:

DIRECTEndotox inComplement

INDIRECTFai lure to maintain n orm al Na+, K+or Ca2+gradientDecreased oxidat ive pho sph orylat ion

OSMOTICGRADIENT

Water entryinto cell

CELLULAREDEMA

IMPAIREDINTRACELLULAR

METABOLISM

Na+ entryinto cell


EFEK SHOCK PADA TINGKATAN


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KidneyOligur ic renal fa i lureHigh outpu t renal fa i lure

LiverLiver fa i lure

GI tractFailure of intest inal barrier (seps is, bleedin g)

LungCapi l lary leak associated w ith or c aused by s epsis andinfect ion

EFEK SHOCK PADA TINGKATANORGAN

TENSION PNEUMOTHORAX


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PRINSIP RESUSITASI

Mempertahankan ventilasi

Meningkatkan perfusi

Terapi penyebab

MAINTAIN VENTILATION


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MAINTAIN VENTILATIONIncreased oxygen

demand

Hyperventilation

Respiratory failureRespiratory acidosis, lethargy-coma, hypoxia

Especially in:

SepsisHypovolemia

Trauma

Respiratory fatigueDiversi blood flow from

vital organ

Organ injury

TREATMENT OF RESPIRATORY FAILURE


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Hypovolemia (blood loss)

Decreased CO

Decreased oxygen delivery, increased

oxygen requirement

Metabolic acidosis, hypoxemia tachypneaTREATMENT:

Primary resuscitationOxygen

Mechanical ventilation if needed

TREATMENT CONCEPT OF SHOCK


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ENHANCING PERFUSION / OXYGEN DELIVERY

Oxygen delivery/DO2=HR X SV X Hb X S02 X 1.34 + Hb X paO

Cardiacoutput

Arterial O2content

Fluids Transfuse Partiallydependent on

FIO2 andpulmonary

status

Inotropes

DO2 = CO x CaO2


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SUMMARY

Shock is an altered state of tissueperfusion severe enough to inducederangements in normal cellular function

Neuroendocrine, hemodynamic andmetabolic changes work together torestore perfusion

Shock has many causes and often maybe diagnosed using simple clinicalindicators

Treatment of shock is primarily focusedon restoring tissue perfusion and oxygendelivery while eliminating the cause

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16. Manajemen Shock.ppt