Download - 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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Inotropic / Vasopressor Agents
Norepinephrine
0.05 g/kg/min and titrate to effect
Inotropic and vasopressor effects
Potent vasopressor at high doses
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Inotropic / Vasopressor Agents
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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EFEK SHOCK PADA TINGKATAN SEL
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.
EFEK SHOCK PADA TINGKATAN SEL
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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 SEL
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