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

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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: 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

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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 pulmonary embolus

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CARDIOGENICCARDIOGENIC

HYPOVOLEMICHYPOVOLEMIC

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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

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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

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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

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Cont…

• Correct hypotension first

• Decrease heart rate

• Correct hypoperfusion

abnormalities

• Monitor for deterioration of oxygenation

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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

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Cont….

• Dobutamine

– 5-20 g/kg/min

– Inotropic and variable chronotropic effects

– Decrease in systemic vascular resistance

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Cont…..

• Norepinephrine

– 0.05 g/kg/min and titrate to effect

– Inotropic and vasopressor effects

– Potent vasopressor at high doses

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Cont…..

• Epinephrine

– Both and actions for inotropic and vasopressor effects

– 0.1 g/kg/min and titrate

– Increases myocardial O2 consumption

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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 more chronotropic benefit

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

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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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