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SYOKSYOK
Pelatihan Perawat RSRPMedan-2014
DEFINIDEFINISISI
IT IS NOT LOW BLOOD PRESSURE !!!IT IS HYPOPERFUSION…..
Gangguan dari perfusi jaringan yang Gangguan dari perfusi jaringan yang terjadi akibat adanya terjadi akibat adanya
ketidakseimbangan antara suplai ketidakseimbangan antara suplai oksigen ke sel dengan kebutuhan oksigen ke sel dengan kebutuhan
oksigen dari sel tersebut. oksigen dari sel tersebut. Semua jenis syok mengakibatkan Semua jenis syok mengakibatkan
gangguan pada perfusi jaringan yang gangguan pada perfusi jaringan yang selanjutnya berkembang menjadi gagal selanjutnya berkembang menjadi gagal
sirkulasi akut atau disebut juga sirkulasi akut atau disebut juga sindroma syoksindroma syok
Shock Categories
• Cardiogenic
• Hypovolemic
• Distributive
• Obstructive
®
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: mental status change, oliguria, acidosis
Cardiogenic Shock
• Decreased contractility
• Increased filling pressures,
decreased LV stroke work, decreased cardiac output
• Increased systemic vascular resistance compensatory
Hypovolemic Shock
• Decreased cardiac output
• Decreased filling pressures
• Compensatory increase in systemic vascular resistance
®
Distributive Shock
• Normal or increased cardiac output
• Low systemic vascular resistance
• Low to normal filling pressures
• Sepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency
®
Obstructive Shock
• Decreased cardiac output• Increased systemic vascular
resistance• Variable filling pressures
dependent on etiology• Cardiac tamponade, tension
pneumothorax, massive pulmonary embolus
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CARDIOGENICCARDIOGENIC
HYPOVOLEMICHYPOVOLEMIC
OO22
OO22
OBSTRUCTIVEOBSTRUCTIVE
SEPTICSEPTIC
PATOFISIOLOGI DARI RESPON PATOFISIOLOGI DARI RESPON TUBUH TERHADAP SHOCKTUBUH TERHADAP SHOCK
Respon NeuroendokrinRespon Neuroendokrin
Respon HemodinamikRespon Hemodinamik
Respon MetabolikRespon Metabolik
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HYPOVOLEMIAHYPOVOLEMIA
R atriumR atriumlow-pressure stretch low-pressure stretch
receptorsreceptors
Aorta/carotidsAorta/carotidsHigh-pressure High-pressure baroreceptorsbaroreceptors
LOSS OF TONIC LOSS OF TONIC INHIBITION OF INHIBITION OF CENTRAL AND CENTRAL AND SYMPATHETIC SYMPATHETIC
NERVOUS SYSTEMSNERVOUS SYSTEMS
RenalRenal Renin releaseRenin release
Pituitary glandPituitary glandACTH, ADH and GH releaseACTH, ADH and GH release
Adrenal gland (medulla)Adrenal gland (medulla)Epinephrine/norepinephrine Epinephrine/norepinephrine
releaserelease
Adrenal cortexAdrenal cortexCortisol releaseCortisol release
Adrenal cortexAdrenal cortexAldosterone releaseAldosterone release
Angiotensin IIAngiotensin IIDecreased renal Decreased renal perfusionperfusion
FEARFEARStimulation of limbic Stimulation of limbic
area of brainarea of brain
IncreasedIncreased: : hypothalamic, hypothalamic,
adrenomedullary adrenomedullary adrenocortical activityadrenocortical activity
Neuroendocrine Neuroendocrine ResponsRespons
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Haemodynamic ResponsVenoconstriction
Sympathetic n. system (SNS)Catecholamines (CA)Angiotensin II (ATII)
ADH
Reduced venous capacitance
Arteriolar constrictionSNS, CA, ATII, ADH
Decreased capillary P
Fluid shift from interstitium into vascular compartment
Increased distal tubular reabsorption
Aldosterone, ADH
Increased proximal tubular reabsorption
SNS, CA, ATII
Increased myocardial contractility
SNS, CA
Restoration of blood volume
Increased ventricular filling
P
Increased ventricular ejection fraction
SV
CO
BP
Increased SVR due to arteriolar construction
SNS, CA, ATII, ADH
SVR
Release of :CatecholaminesCortisolGlucagon
LIPOLYSIS
INCREASE IN PLASMA FREE FATTY ACIDS
Metabolic Respons
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RESPON METABOLIKRESPON METABOLIK
HyperglikemiaHyperglikemia
Mobilisasi lemakMobilisasi lemak
Katabolisme/pemecahan ProteinKatabolisme/pemecahan Protein Peningkatan sintesis ureaPeningkatan sintesis urea Peningkatan asam amino Peningkatan asam amino
aromatikaromatik
Penurunan sintesis reactan fase Penurunan sintesis reactan fase akutakut
Peningkatan osmolalitas ekstraselPeningkatan osmolalitas ekstrasel
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RESPON METABOLIKRESPON METABOLIK
Breakdown of Breakdown of skeletal skeletal
muscle into muscle into a.a.a.a.
ConversioConversion of a.a. n of a.a.
to glucoseto glucose
Release of:Release of:CatecholaminesCatecholaminesCortisolCortisolGlucagonGlucagonGrowth hormoneGrowth hormone
Impaired Impaired peripheral peripheral
glucose glucose uptakeuptake
HYPERGLYCEMIHYPERGLYCEMIAA
Glycogen Glycogen breakdowbreakdow
nn
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METABOLIC RESPONSMETABOLIC RESPONSDecreased blood Decreased blood
volumevolume
Decreased CODecreased CO
Cellular hypoperfusion and hypoxiaCellular hypoperfusion and hypoxia
Anaerobic glycolysisAnaerobic glycolysisPyruvate converted to lactic acidPyruvate converted to lactic acid
METABOLIC ACIDOSISMETABOLIC ACIDOSIS16
Mekanisme untuk memperbaiki Mekanisme untuk memperbaiki keseimbangankeseimbangan
kardiovaskulerkardiovaskuler
Redistribusi aliran darah Redistribusi aliran darah
Peningkatan “cardiac outputPeningkatan “cardiac output
Memperbaiki volume intravaskularMemperbaiki volume intravaskular
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STIMULASI NEUROENDOKRINSTIMULASI NEUROENDOKRIN
HYPOTENSIONHYPOTENSION
BLOOD FLOW BLOOD FLOW PROTECTEDPROTECTED
HeartHeartBrainBrain
Adrenal/pituitary glandAdrenal/pituitary gland
BLOOD FLOW BLOOD FLOW DECREASEDDECREASED
SkinSkinMuscleMuscle
Splanchnic circulationSplanchnic circulation
REDISTRIBUSI REDISTRIBUSI ALIRAN DARAHALIRAN DARAH
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CARDIAC OUTPUT CARDIAC OUTPUT = = HR X HR X SVSV
SympatheticSympathetic n. systemn. system
Catecholamine Catecholamine releaserelease
Increase EDV via:Increase EDV via:VenoconstrictionVenoconstriction
Arteriolar constrictionArteriolar constrictionRenal reabsorptionRenal reabsorption
Increased Increased contractilitycontractility
Limited to 180 Limited to 180 beats/min before beats/min before
decreased CO due to decreased CO due to decreased diastolic decreased diastolic
filling timefilling time
PENINGKATAN PENINGKATAN CARDIAC OUTPUT CARDIAC OUTPUT
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MEMPERBAIKI VOLUME MEMPERBAIKI VOLUME DARAHDARAH
Transcapillary refill phaseTranscapillary refill phase1. Decreased capillary pressure caused by hypotension1. Decreased capillary pressure caused by hypotension
2. Sympathetic increase in precapillary arteriolar constriction2. Sympathetic increase in precapillary arteriolar constriction
Decrease capillary hydrostatic pressure promotes passage of fluid Decrease capillary hydrostatic pressure promotes passage of fluid from interstitium to intravascular spacefrom interstitium to intravascular space
Plasma protein restitution phasePlasma protein restitution phaseIncreased plasma osmolarity due to Increased plasma osmolarity due to mainlymainly hepatic release of hepatic release of
glucose, pyruvate, amino acids, etc.glucose, pyruvate, amino acids, etc.
Increased interstitial osmolarityIncreased interstitial osmolarity
Increased interstitial volume and pressureIncreased interstitial volume and pressure
Transcapillary movement of albumin into intravascular spaceTranscapillary movement of albumin into intravascular space20
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EFEK SHOCK PADA TINGKATAN EFEK SHOCK PADA TINGKATAN SELSEL
HYPOXIAHYPOXIA
LOW-FLOW,LOW-FLOW,POOR PERFUSIONPOOR PERFUSION
ANAEROBIC METABOLISM
ACIDOSIS
DECREASED CELLULAR ENERGY EFFICIENCY
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:
• DIRECT EndotoxinComplement• INDIRECTFailure to maintain normal Na+, K+ or Ca2+ gradientDecreased oxidative phosphorylation
OSMOTIC GRADIENT
Water entry into cell
CELLULAR EDEMA
IMPAIRED INTRACELLULAR
METABOLISM
CELL
DEATH
Na+ entry into cell
EFEK SHOCK PADA TINGKATAN EFEK SHOCK PADA TINGKATAN SELSEL
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KidneyKidney Oliguric renal failureOliguric renal failure High output renal failureHigh output renal failure
LiverLiver Liver failureLiver failure
GI tractGI tractFailure of intestinal barrier (sepsis, bleeding)Failure of intestinal barrier (sepsis, bleeding)
LungLung Capillary leak associated with or caused by sepsis and Capillary leak associated with or caused by sepsis and
infectioninfection
EFEK SHOCK PADA TINGKATAN ORGANEFEK SHOCK PADA TINGKATAN ORGAN
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STAGES OF SHOCK
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COMPENSATED SHOCK
Body defense mechanisms attempt
to preserve major organs✓Precapillary sphincters close,
blood is shunted✓Increased heart rate and strength
of contractions✓Increased respiratory function,
bronchodilation
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……COMPENSATED SHOCK
Will continue until problem solved or
shock progresses to next stage
Can be difficult to detect with subtle
indicators✓Tachycardia✓Decreased skin perfusion✓Alterations in mental status
Some medications such as propranolol
can hide signs and symptoms
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UNCOMPENSATED SHOCK
Physiological response✓Precapillary sphincters open, blood pressure falls✓Cardiac output falls✓Blood surges into tissue beds,
blood flow stagnates✓Red cells stack up in rouleaux
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……UNCOMPENSATED SHOCK
Easier to detect than compensated
shock✓Prolonged capillary refill time✓Marked increase in heart rate✓Rapid thready pulse✓Agitation, restlessness, confusion
Decompensation
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IRREVERSIBLE SHOCK
Compensatory mechanisms fail,
cell death begins, vital organs
falter
Patient may be resusitated but
will die later of (ARDS, renal and
liver failure, sepsis)
Clinical Differentiation Shock
Hemorrhagic Shock Non Hemorrhagic Shock✔Cardiogenic ✔Tension pneumothorax ✔Neurogenic ✔Septic ✔Anaphylactic
Hemorrhagic ShockHemorrhagic Shock
Paling sering terjadi terutama pada kasus trauma
Dijelaskan secara khusus pada Modul 5 (Terapi Cairan 1)
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….Syok Perdarahan
Non Hemorrhagic Non Hemorrhagic ShockShock
Cardiogenic Shock Myocardial dysfunction
✓Blunt cardiac trauma
✓Cardiac tamponade
✓Air embolism
✓Valve rupture
ECG monitoring
Isoenzynme-CPK
Echocardiography
✓Tachycardia✓ Blowing heart sound✓ Venectasia regio colli✓ Hypotension
Pumpin
g
dysfu
nctio
n
Dimin
ished b
lood
retu
rn to
the
heart
Riwayat kejadianTrauma torak : tumpul, tajam
Disfungsi miokard Kontusio, disritmia, emboli udara, infark, tamponade
EKG monitoringUltrasonografiPemasangan CVPPemeriksaan laboratoriumPerikardiosentesis
….Syok Kardiogenik
✔Trauma torak : tajam, tumpul✔Takikardia✔Hipotensi/syok✔Vena leher meninggi✔Suara jantung menjauh✔EKG low voltage✔Ultra sonografi✔Perikardiosentesis
Tamponade Jantung
✓Ventil mechanism/flap-valve
✓Sesak nafas , RR >
✓Emphysema subcutan
✓Perkusi hypersonor
✓Suara paru menghilang pada ipsilateral
✓Trakhea terdorong kontralateral
✓Tachycardia
✓Hypotension
Tension Pneumothorax
★
Med
iast
inum
terg
eser
★
Venou
s re
turn
terg
anggu
★
Pumpin
g terg
anggu
✔Mirip tamponade jantung
✔Peningkatan tekanan intra pleural
✔Pergeseran mediastinumVenous return
Pre load
Cardiac output
✔Pergeseran trakhea
✔Paru kolaps, suara napas hilang
✔Perkusi hipersonor
✔Dekompresi pleura JarumChest tube
Pneumothoraks tension
Punksi pleura untuk dugaan pneumothorax (sistim jarum + spuit + air)
NEEDLE THORACOSYNTHESIS
Neurogenic Shock Spinal Shock
✓Cedera tulang belakang
✓Cedera medulla spinalis
✓Sympathetic denervasi
✓Vasodilatasi, gambaran hypovolemia
✓No tachycardia,
✓No vasokonstriksi
Hyp
oten
si,
Shoc
k
Perife
r ha
ngat
Inap
prop
riat
e
vaso
dila
tation
Inad
equa
te p
ump
func
tion
….Neurogenik Syok….Neurogenik Syok✔Perdarahan otak tak shock !!!✔Cedera tulang leher (spinal cord)✔Kehilangan tonus simpatis
HipotensiVasodilatasiNadi Tekanan nadi lebar
✔Pemberian volume✔Monitoring CVP✔Vasopressor/Atropin
Septic Shock
Jarang terjadi segera setelah trauma
Dapat terjadi pada kasus trauma yang
terlantar
Luka tembus abdomen, perforasi
Shock septik pada periode awal :✔Tachycardia✔Perifer hangat✔Sistolik bisa normal✔Pulse pressure lebar In
adeq
uate
pum
p
func
tion
Inap
prop
riate
vaso
dila
tatio
n
….Septik Syok….Septik Syok
✔Jarang pada awal trauma✔ Fase awal
Kulit hangatTekanan nadi lebar
✔Bila tak febris, sulit dibedakan dgn syok hipovolemik✔ Kontaminasi perforasi usus (trauma abdomen)
SYOK ANAFILAKSIS
MENDADAK, TAK DAPAT DIRAMALKAN KEMATIAN DALAM WAKTU SINGKAT
SYOK (HIPOVOLEMIK) GAGAL NAFAS AKUT
Anaphylactic Shock
Reaksi Anafilaktik1. Adrenalin (1 ampul = 1 mg ) iv – im – sc - sl - transtracheal - et
Berat : 0.50 - 1 ampulSedang : 0.25 – 0.50 ampulRingan : tanpa shock - tidak perlu
2. Baringkan penderita, kedua tungkai angkat keatas (Shock Position)Jaga jalan nafas tetap bebasO2 masker 10 lpm, bila ada.Siap Ambu Bag, siap beri nafas buatan , siap RJPOLIHAT : gerak dada, ada nafas ?DENGAR : suara nafas, tensi. Ada nafas ? Shock ?RABA : hawa nafas, perfusi perifer. Ada nafas ? Shock?Pasang Infus : RL/ PZ grojok 500-1000 cc
3. 5-10 menit kemudiank/p ulangi AdrenalinBeri Oradexon iv 1-2 ccatau Dexamethason 100-200mg imAvil/ Delladryl 1 cc im, hati-2 tensi turun lagi
4. Bila ada wheezing beri aminofilin iv pelan 5-10 cc ( 1Ampul )Hati-hati bila tensi < 100 mmHg, K/P pemberian dg titrasi.
Laki-laki 50 th KP Fisik baik Tensi/Nadi baikRiwayat alergi (-) sesak (-) asthma (-)
disuntik streptomycine - Penicillin
Shock : nadi kecil cepat perfusi dingin pucat basah, sesak hebat, pasien gelisah
KASUS
Time Saving is Life Saving
Initial AssesmentInitial Assesment Airway , Breathing ok?Airway , Breathing ok?
CirculationCirculation✓HR within normal limit
✓Pulse pressure WNL
✓Warm, Pink, Dry
NO SHOCK
Initial AssesmentInitial Assesment Airway , Breathing ok?Airway , Breathing ok?
CirculationCirculation✓Tachycardia
✓Cutaneous vasoconstriction
✓Pulse pressure
✓Calmy
SHOCK
PRINSIP PRINSIP RESUSITASIRESUSITASI
Mempertahankan Mempertahankan ventilasiventilasi
Meningkatkan Meningkatkan perfusiperfusi
Terapi penyebabTerapi penyebab
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MAINTAIN MAINTAIN VENTILATIONVENTILATIONIncreased oxygen Increased oxygen
demanddemand
HyperventilationHyperventilation
Respiratory failureRespiratory failureRespiratory acidosis, lethargy-coma, hypoxiaRespiratory acidosis, lethargy-coma, hypoxia
Especially in:Especially in:SepsisSepsis
HypovolemiaHypovolemiaTraumaTrauma
Respiratory fatigueDiversi blood flow from
vital organ
Organ injury
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Hypovolemia (blood Hypovolemia (blood loss)loss)
Decreased CO Decreased CO
Decreased oxygen delivery, Decreased oxygen delivery, increased oxygen requirementincreased oxygen requirement
Metabolic acidosis, Metabolic acidosis, hypoxemia ,tachypneahypoxemia ,tachypnea
TREATMENT:TREATMENT:Primary resuscitationPrimary resuscitation
OxygenationOxygenationMechanical ventilation if neededMechanical ventilation if needed
TREATMENT OF TREATMENT OF RESPIRATORY FAILURERESPIRATORY FAILURE
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TREATMENT CONCEPT TREATMENT CONCEPT OF SHOCKOF SHOCK
ENHANCING PERFUSION / OXYGEN DELIVERYENHANCING PERFUSION / OXYGEN DELIVERY
Oxygen delivery/DOOxygen delivery/DO22 == HR X SVHR X SV X X Hb X S0Hb X S02 2 X 1.34 + Hb X paOX 1.34 + Hb X paO22
Cardiac Cardiac outputoutput
Arterial OArterial O22 contentcontent
FluidsFluids TransfuseTransfuse Partially Partially dependent on dependent on
FIOFIO22 and and pulmonary pulmonary
statusstatus
InotropesInotropes
DO2 = CO x CaO2
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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
Cardiac Output x SVR
Pipe = VascularPump =Heart
Volume =Blood
Hypovolemic Shock
Cardiogenic Shock
Distributive Shock
Inotropes (Dob,Dop,Adr,Amr)
Vasopressor ( NE,PE,Adr,Dop)
Fluids
Obstructive Shock
Release tamponade,etc
Blood Pressure
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Cardiogenic Shock Management
• Treat arrhythmias
• Diastolic dysfunction may require increased filling pressures
• Vasodilators if not hypotensive
• Inotrope administration
Cont…..
• Vasopressor agent needed if hypotension present to raise aortic diastolic pressure
• Consultation for mechanical assist device
• Preload and afterload reduction to improve hypoxemia if blood pressure adequate
Hypovolemic Shock Management
• Volume resuscitation – crystalloid, colloid
• Initial crystalloid choices– Lactated Ringer’s solution– Normal saline (high chloride may
produce hyperchloremic acidosis)• Match fluid given to fluid lost
– Blood, crystalloid, colloid
®
Distributive Shock Management
• Restore intravascular volume
• Hypotension despite volume therapy
– Inotropes and/or vasopressors
• Vasopressors for MAP < 60 mm Hg
• Adjunctive interventions dependent on etiology
®
Obstructive Shock Treatment
• Relieve obstruction
– Pericardiocentesis
– Tube thoracostomy
– Treat pulmonary embolus
• Temporary benefit from fluid or inotrope administration
Fluid Therapy• Crystalloids
– Lactated Ringer’s solution– Normal saline
• Colloids– Hetastarch– Albumin– Gelatins
• Packed red blood cells• Infuse to physiologic endpoints
®
Cont…
• Correct hypotension first
• Decrease heart rate
• Correct hypoperfusion
abnormalities
• Monitor for deterioration of oxygenation
®
How Much Fluid To How Much Fluid To Give?Give? Some measure of intravascular fillingSome measure of intravascular filling
Pressure (CVP or PAOP) Pressure (CVP or PAOP) Some assessment of risk of pulmonary oedema Some assessment of risk of pulmonary oedema
and capillary leakand capillary leakPulmonary gas exchange (PaO2:FiO2)Pulmonary gas exchange (PaO2:FiO2)Requirement for positive pressure (PEEP)Requirement for positive pressure (PEEP)Chest X-rayChest X-ray
Some assessment of response to treatmentSome assessment of response to treatmentChanges in acid base balance, lactateChanges in acid base balance, lactateMeasurement of cardiac outputMeasurement of cardiac output
Inotropic / Vasopressor Agents• Dopamine
– Low dose (2-3 g/kg/min) – mild inotrope plus renal effect
– Intermediate dose (4-10 g/kg/min) –inotropic effect
– High dose ( >10 g/kg/min) –vasoconstriction
– Chronotropic effect
®
Cont….
• Dobutamine
– 5-20 g/kg/min
– Inotropic and variable chronotropic effects
– Decrease in systemic vascular resistance
®
Cont…..
• Norepinephrine
– 0.05 g/kg/min and titrate to effect
– Inotropic and vasopressor effects
– Potent vasopressor at high doses
®
Cont…..
• Epinephrine
– Both and actions for inotropic and vasopressor effects
– 0.1 g/kg/min and titrate
– Increases myocardial O2 consumption
®
Pediatric Considerations
• BP not good indication of hypoperfusion
• Capillary refill, extremity temperature bettersigns of poor systemic perfusion
• Epinephrine preferable to norepinephrine due to more chronotropic benefit
• Fluid boluses of 20 mL/kg titrated to BP or total 60 mL/kg, before inotropes or vasopressors
®
Pediatric Considerations
• Neonates – consider congenitalobstructive left heart syndrome as cause of obstructive shock
• Oliguria
– <2 yrs old, urine volume <2 mL/kg/hr
– Older children, urine volume <1 mL/kg/hr
What Do You Need to Know What Do You Need to Know When You Resuscitate a When You Resuscitate a Patient in Shock?Patient in Shock? Arterial blood pressureArterial blood pressure Urine outputUrine output Systemic acid–base balance (pH, SBE, lactate)Systemic acid–base balance (pH, SBE, lactate) Some clinical assessment of tissue perfusionSome clinical assessment of tissue perfusion
““warm and well perfused” or “cold and shut down”warm and well perfused” or “cold and shut down” Some measurement of global blood flow and tissue Some measurement of global blood flow and tissue
perfusionperfusion Cardiac output or cardiac indexCardiac output or cardiac index
Arterial oxygen delivery, oxygen uptake indexArterial oxygen delivery, oxygen uptake index Mixed venous saturation and PvO2Mixed venous saturation and PvO2
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SUMMARYSUMMARY Shock is an altered state of tissue Shock is an altered state of tissue
perfusion severe enough to induce perfusion severe enough to induce derangements in normal cellular derangements in normal cellular functionfunction
Neuroendocrine, hemodynamic Neuroendocrine, hemodynamic and metabolic changes work and metabolic changes work together to restore perfusiontogether to restore perfusion
Shock has many causes and often Shock has many causes and often may be diagnosed using simple may be diagnosed using simple clinical indicatorsclinical indicators
Treatment of shock is primarily Treatment of shock is primarily focused on restoring tissue focused on restoring tissue perfusion and oxygen delivery perfusion and oxygen delivery while eliminating the causewhile eliminating the cause
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