2010 Penatalaksanaan Syok Pada Anak
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PENATALAKSANAAN SYOK
PADA ANAK
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PENDAHULUAN
SINDROM KLINISKEGAGALAN SISTEM SIRKULASI
KEBUTUHAN OKSIGEN NUTRIEN JARINGAN
DEFISIENSI AKUT DITINGKAT SEL
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SYOK PADA ANAK : Keadaan gawat darurat
morbiditas / mortalitas 80 % hipovolemik Syok kompensasi sulit di D / o.k
manifestasi klinis tak jelas ( refleks simpatis Redistribusi selektif al. daerah dari organ perifer non-vital ke jantung, paru, otak )
Tujuan Primer Pengelolaan Syok :- Preload ( resusitasi volume )- Kontraktilitas - Resistensi pada sistemik
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DEFINISI SYOK
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM SIRKULASI UNTUK MENCUKUPI :
NutrisiOksigen
Pasokanutilisasi
Metabolisme Jaringan tubuh
Defisiensi 02 Seluler
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FUNGSI SISTEM SIRKULASI
Jantung Pembuluh
Darah Volume Darah
Curah jantung & adekuatAliran darah
Metabolisme
jaringan
Metabolit
Eliminasi Di Organ
Pembuangan
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PENGATURAN CURAH JANTUNG DAN TEKANAN DARAH
PRELOAD CONTRACTILITY AFTERLOAD
HEART RATE STROKE VOLUME
CARDIAC OUTPUT SYSTEMIC VASCULAR RESISTANCE
BLOOD PRESSURE
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PENGANGKUTAN OKSIGEN
Cardiac Out Put Blood flow
OxygenDelivery
Blood O2 Content
Hb Contentration
O2 Bound to Hb
O2 Dissolved in Plasma
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KLASIFIKASI SYOK MENURUT ETIOLOGI
SYOK HIPOVOLEMIK SYOK DISTRIBUTIF SYOK KARDIOGENIK SYOK SEPTIK SYOK OBSTRUKTIF
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STADIUM SYOKFASE I : KOMPENSASI
• Mekanisme Kompensasi Tubuh refleksi simpatis
- Resistensi sistemik : HR; kulit dingin, pucat, cap.refill
terlambat, nadi lemah, tek.nadi sempit-
Tekanan darah ( N ) - Tekanan Diastolik - Resistensi pembuluh darah
splanknik ↑: Ginjal (Diuresis <), Saluran cerna (muntah, ileus)
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FASE II : DEKOMPENSASI (1)
- Mekanisme kompensasi gagal
- Metabolisme anaerobik- Asam laktat asidosis >> terbentuk asam karbonat intraseluler- Kontraktilitas otot jantung - Pompa Na – K sel
Integritas membran sel
Kerusakan sel
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FASE II : DEKOMPENSASI (2)
Aliran darah lambat
Agregasi TrombositPembentukan Trombus
PendarahanPelepasan Mediator
Vasodilatasi Arterial
Kenaikan Permeabilitas Kapiler
VR
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Fase dekompensasi
• Perfusi jaringan indekuat disertai hipotensi
• Kesadaran menurun krn perfusi ke otak menurun
• Hipotensi sebagai tanda terakhir dari syok• Untuk anak 1-10th: <70 mmHg +(umur/thn
x 2) mmHg
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FASE III : IREVERSIBEL
Kerusakan / Kematian Sel Disfungsi sistem multi organ Cadangan fostat E. Tinggi
( Hepar, Jantung )
Tekanan darah tak terukur Nadi tak teraba
Kesadaran AnuriaGMO
klinis
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PERJALANAN PATOFISIOLOGI SYOK
Septic Shock
Cardiogenic ShockHypovolemic
ShockCapillary Leak
Mediators
Myocardial Depression
Preload Vasodilatation
Contractility
Cardiac Output Blood Pressure
Sympathetic Discharge
Vasoconstriction,
HR Contractility
Improved Cardiac output and blood pressure
COMPENSATED
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DECOMPENSATED
Myocardial perfusion Myocardial O2
Consumption
Cardiac Output
Mediator Release
Cell Function
Cell Death Death of Organism
Tissue Ischemia
Loss of Auto regulation of
Microcirculation
COMPENSATED
Vasoconstriction HR Contractility
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Syok Hipovolemik
• Etiologi: Diare, perdarahan, muntah, intake tak adekuat, diuresis osmotik, luka bakar
HYPOVOL
SHOCK
PRELOAD ↓
AFTERLOAD ↑
CONTRACTILITYN / ↑
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Syok hipovolemik Primary Assessment: Finding• A
• B Takhipneu tanpa pe↑ WOB• C Takhikardi
Tek.Drh N/ hipotensi dgn
tek.nadi sempit
Nadi lemah,kecil /tak teraba
Pengisian kapiler lambat
kulit dingin,pucat
Kesadaran menurun
Oliguria
D Kesadaran menurun
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Distributive Shock
Distributiveshock
PRELOAD N / ↑
CONTRACTILITYN / ↓
AFTERLOADVariable
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Findings of Distributive Shock
• Primary Assessment Finding• A Patent airway, unless unconc.• B Tachypnea without ↑WOB, except
caused by pneumonia, ARDS, pulm edema• C Tachycardia, Hypotension with wide
pulse pressure(warm shock) or narrow p.pressure(cold shock) or normotension; Bounding perpheral pulse, Delayed cap.refill, Warm&flush skin(warm shock) or pale skin(cold shock): Changes in mental status; oliguria
• D Changes in mental status
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Septic Shock
PRELOAD↓↓
CONTRACTI-LITY ↓/ N
AFTERLOAD VARIABLE
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Consensus Definitions and clinical Characteristic of Ped.Sepsis
• Systemic Inflammatory Response Syndrome ( SIRS )
• Sepsis• Severe Sepsis• Septic shock
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SIRS
• Core temp of >38.5°C or <36°C• Tachycardia >2SD above normal for age,
for chhildren <1 year bradycardia <10th percentile for age
• Mean RR>2SD above normal for age• Leucocyte count ↑ or ↓ for age or 10%
immature neutrophils• ( At least 2 of the 4 criteria )
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• SEPSIS :
SIRS in the presence of, or as a result of, suspected or proven infection
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Severe sepsis
• Sepsis plus either cardiovascular dysfunction or ARDS
Or• Sepsis plus 2 or more other organ failures
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RF as sign of organ dysfunctionin sepsis
• PaO2/FiO2 <300 in absence of CHD or lung disease
• PaCO2 >65 mmHg or 20 mmHg above baseline
• Proven need FiO2 >50% to maintain SaO2 >92%
• Need nonelective MV (invasive or noninvasive)
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Septic shock
• Sepsis and
• Cardiovascular dysfunction despite administration of isotonic iv boluses > 40 ml/kg in 1 hour
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Cardiovascular dysfunction
• Hypotension (SBP <5th percentile for age or SBP <2SD below normal for age or
• Need for vasoactive drug to maintain BP in normal range or
• Two of the following characteristic of inadequate organ perfusion:
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Inadequate organ perfusion
• Unexplained metabolic acidosis: base deficit < 5meq/l
• Increase arterial lactate > twice the upper limit of normal
• Oliguria: Urine output0.5 ml/kg/hour• Prolonged cap refill: > 5 second• Cor to peripheral temp gap > 3°C
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SEPTICSHOCK
PRELOADDECREASE
CONTRACTILITYN / DECREASED
AFTERLOADVARIABLE
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III. SYOK KARDIOGENIK
Etiologi : Pasca Bedah Penyakit Jantung Bawaan Miokarditis Infark / Iskemik Jantung Kardiomiopati Primer / Sekunder Hipoglikemia, Gangguan Metabolik Asfiksia, Sepsis
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CARDIOGENICSHOCK
PRELOADVARIABLE
CONTRACTILITYDECREASED
AFTERLOADINCREASED
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MEKANISME SYOK KARDIOGENIK
Cardiogenic Shock
Contractility
CO BP
Metabolic acidosis, hypoxia,Myocardial depressant factor
Compensatory mech. Afterload SVR
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SYOK KARDIOGENIK
• Cardiac Ventricular Performance • Factor Determinant :
a. Frekuensi dan Irama Jantungb. Preload dan Afterloadc. Kontraktilitas Miokard
• Kompensasi Tubuh Self Perpetuating Cycle
Syok Progresif Memburuk
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Findings of Cardiogenic Shock• Primary Assessment Finding• A• B Tachypnea; WOB↑• C Tachycardia; N/low BP with
a narrow pulse pressure; weak or absent of peripheral pulse; N and then weak central pulses;Delayed cap refill with cool extremities; Signs of CHF; cyanosis(CHD/pulm.edema); End-organ Function ( Cold, pale skin, oliguria)
• D Changes of mental status
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Obstructive Shock
• Cardiac tamponade• Tension pneumothorax• Ductal – dependent congenital heart lesions• Massive pulmonary embolism
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Cardiac tamponade
• Muffled or diminished heart sound• Pulsus paradoxus(decrease in systolic BP
by more than 10 mmHg during inspiration• Distended neck vein• Note: Children following cardiac surgery,
D/ ndistinguishable from cardiogenic shock, Echo: important
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Tension pneumothorax
• Patients with chest trauma, or any intubated child who deteorates suddenly during PPV
• Hyperresonance on the affected side• Diminished breath sounds on the affected side• Distended neck vein• Tracheal deviation towards contralateral side• Rapid deteoration in perfusion and rapi change
from tachycardia to bradicardia
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Pathogenesis and Pathophysiology of SepsisNew Concept about SIRS, SEPSIS, CARS, MARS
Pro-inflammatory response
Anti-inflammatory response
Systemic Reaction:SIRS (pro-inflammatory)
CARS (anti-inflammatory)MARS (mixed)
Systemic spillover of pro-inflammatory
mediators
Systemic spillover of anti-inflammatory
mediators
Initial insult (bacteria, viral, traumatic, thc, mal)
Cardiovascular Compromise
shock, SIRS pre-dominates
Homeostasis
CARS and SIRSbalanced
Apoptosis (cell death)
Death with minimal
inflammation
Organ dysfunction
SIRSPre-dominated
Suppression of the immune
systemCARS
pre-dominated
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SEPSIS DAN GANGGUAN KOAGULASI
Sepsis
Inflammatory cytokines
IL - 6 TNF -
Tissue factor Mediated
activation of coagulation
Inhibition of physiological anticoagulant
pathways
Depression of
fibrinolysis due to high
levels of PAI-1Enhanced fibrin
formationImpaired fibrin
removal
Microvascular thrombosis
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CYTOKINE-MEDIATED PATHOGENETIC PATHWAYS of MICROVASCULAR
THROMBOSIS in SEPSIS
Sepsis
Activation of coagulation
Widespread fibrin
Deposition
Consumption of platelets and clotting
factorMicrovascular
thrombosis Bleeding (severe)
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MANIFESTASI KLINIS SYOK SEPTIK
STADIUM KOMPENSASI- Resistensi Vaskuler - Curah Jantung - Takhikardia- Ekstermitas Hangat- Divresis Normal
STADIUM DEKOMPENSASI- Volume Intravaskuler - Depresi Miokard- Eksternal Dingin- Gelisah, Anuria, Distres Respirasi- Resistensi Vaskuler - Curah Jantung
STADIUM IREVERSIBEL- GMO
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Most Common Pathogens in Childhood Bacterial Sepsis
Age Group Pathogens Antimicrobial(Pending culture)
Initial dose (mg/kg)
0 – 1 months
Group B Strept. EnterobacteriaceaeStaph. AureusListeria meningtides
Ampiciline +GentamicinCefotaxime
502.55-0
1 – 24 months
H. influenzae, Strept. PneumoniaeS. aureus, Neisseria meningtidisGroup B Streptococcus
CefotaximeAmpiciline +Chlorampenicol
505025
> 24 months
S. PneumoniaeH. InfluenzaeS. AureusN. Meningtidis
CefotaximeCefriaxoneAmpiciline +Chlorampenicol
50505025
Immuno compromised
S. aureus, ProteusPseudomonasEnterobacteriaceae
Vancomycin +Ceftazidime +Ticarcillin
255075
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PENATALAKSANAAN SYOK
1. 2.
Oksigenasi
CaO2 SaO2 95 – 100 %
Sistem K.V
a. Preload ( resusitasi volume )
b. Atasi Disritmiac. Koreksi keseimbangan
asam - basaJalan nafas Oksigen Anxietas
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TERAPI CAIRAN PADA SYOK AKSES VENA (90 detik); Tak berhasil IO KRISTALOID dan atau KOLOID
10 – 30 ml / kg B.B (6-10 menit)
diulang 2 – 3 kali SYOK SEPTIK 60 – 100 ml / kg B.B
(dalam 6 jam pertama) THE 1st CONSENSUS CONFERENCE on CCM 1997
(SYOK SEPTIK)a. Koloid terapi inisial, dilanjutkan koloid/kristaloidb. Dipandu : respons klinis,perfusi, perifes, tvs, tekanan sistem,MAP
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Algoritme Terapi Cairan Pada Syok
Suspected shock
Hypovolemia, Hypoperfusion, Tachycardia
10 – 30 mL Cryst/Colloid / kg / 6 – 10 min
Normotensive
Hypotensive
In Sepsis :
Antibiotics, Imunotheraphy
In Anaphylaksis :
Catekolamin, steroid, antihistamin
Urine > 1 ml/kg/hr
10-20 mL crys or coll/kg/10 min
AnuriaUrine < 1 ml/kg/hr
Urine output < 1 ml/kg/hr
Reevaluated
10 mL X.tal/kg
10 mL X.tal/kg
10–20 mL X.tal/kg
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Reevaluated
10 mL X.tal/kg
10 mL X.tal/kg
10-20 mL X.tal/kg
Improved
Reevaluated
Improved
Reevaluated
Hypotensive, urine < 1 mL/kg/hr
CVP < 10 mmHg
CVP, Cardiac status, chest X-Ray, Echocardiography
CVP > 10 mmHg
Afterload reduction, inotropic support, consider pulmonary
10-20 mL X.tal/kg
Reevaluated
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Early Goal DirectedTherapy pada Syok Septik
• Early aggressive fluid therapy (Crystaloid or colloid) In EMU, within 6 hours of admission
• Vasopressors & Inotropic drugs when resistance to fluid therapy
• End points : Good peripheral perfusion Conciousness, Capillary feeling time < 2”, Warm extremities, MAP/Pulse pressure N for age, CVP 8-12 mmHg, Diuresis > 2ml/kg SvcO2 > 70%
• Admission to PICU when stabilized
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Supplemental oxygen endotracheal intubation and
mechanical ventilation
Central venous and arterial
catheterization
Sedation, paralysis (if intubated), or both
Goals achieved
ScvO2
MAP
CVP
Hospital admission
8-12 mmHg
≥ 65 and ≤ 90 mmHg
≥ 70%
Yes
No
Crystalloid
Colloid
< 8 mmHg
Vasoactive agents< 65 mmHg
> 90 mmHg
Transfusion of red cells until hematocrit ≥ 30%
Inotropic agents< 70%
Protocol for Early Goal-Directed
Therapy
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Fluid Therapy in Sepsis and Septic Shock
Type of Fluid Colloid
Crystalloid
Volume 60 – 100 ml/kg
(6 hours)
CO , Restore BP MOF
InotropicVasopressor
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(SYOK KARDIOGENIK) : Fluid Chalenge hati – hati :
a. memperbaiki kontraktilitas jantungb. dipantau ketat dengan TVS
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Efek volume infus 1 L koloid pada kompartemen tubuh (70 kg)
Larutan Vol. Plasma Vol. Inters I.Intrasel
Albumin 5% 1000 - -
Hemacel 700 300 -
Gelafundin 1000 - -
Plasmafusin 1000 - -
Dextran 40 1600 (-260) (-340)
Dextran 70 1300 (-130) (-170)
Expafusin 1000 - -
HAES steril 6%
1000 - -
HAES steri10%
1450 (-450) -
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ADRENAL INSUFFISIENSI PADA SYOK
SEPTIKKORTIKOSTEROID
Pada syok septik, bila refrakter thdp dopamin/adrenalin/nor-adrenalin mungkin terjadi INSUFISIENSI ADRENAL Hydrocortisone 50mg (bolus), dilanjutkan 1-2 mg/kgBB/ 24 jam; 5-7 hari
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TERAPI SUPORTIFSubstitusi faktor koagulasi (pada
Hemodilusi/PIM) :- Fresh Frozen Plasma- Cyroprecipitate
Tranfusi Masif setiap 5 – 6 unit PC ditambah 2 unit FFP
Fibrinogen < 100 mg/dl (tak respons terhadap FFP) : - Cyro precipitate 4 unit/10 kg BB
Konsentrat trombosit diberikan : Trombositopeni berat < 30.000 dengan
perdarahan atau tindakan invasif : - Konsentrat Trombosit
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IMUNOTERAPI
• Tranfusi tukar pada sepsis :
- memperbaiki oksigenasi jantung
- mengeluarkan mediator dan endotokin• Immunoglobulin (I.V) pada sepsis• Hemofiltrasi dan Plasmafiltrasi :
– mengeluarkan endotoksin, mediator
– mengurangi respons inflamasi sistemik (SIRS)
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FUNGSI ORGANA. PARU :
Suplai Oksigen adekuat - Intubasi/pemasangan V. mekanik dini
pada syok septik- Pemberian cairan resusitasi, bila terlalu
banyak/ agresif resiko tinggi edema paru
B. OTAK :- Hindari hipoksia, hipoglikemia- Hindari hiperkapnea (dengan ventilator)- Pertahankan perfusi serebral :
a. volume intravaskularb. COc. Hb/tekanan darah adekuat
- Pemantauan kadar Na serum, koreksi hati-hati
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FUNGSI ORGAN (lanjutan)C. SIRKULASI SPLANKHNIK / SALURAN CERNA
- Resusitasi volume, optimalisai CO, tekanan darah- Koreksi hipotensi (vasopresor/inotropik)- NUTRISI ENTERAL DINI
D. GINJAL- Resusitasi volume, optimalisasi CO, tekanan darah- Koreksi hipotensi- Koreksi hipoksia dan anemia berat- Hindari obat-obatan nefrotoksik
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TATALAKSANA SYOK KARDIOGENIK
• Oksigenasi Adekuat• Koreksi GGN Asam Basa dan Elektrolit• Kurangi Rasa Sakit dan Ansietas• Atasi Disritmia Jantung• Kelebihan Preload : Diuretika• Kontraktilitas : Fluid Challenge Sesuai
CVP/POAP Obat Inotropik (+)• Beban Afterload (SVR ) : Vasodilator• Koreksi Penyebab Primer
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Commonly Used Cardiovascular Drugs in Shock Syndromes
Drug Dose (
ug/kg/min )
Comment
Inotropioc agentsNorephrine( - adrenergic )
0.05 – 1.0 For profound hypotension not responding to fluid or other inotropic drugs
Ephinephrine( - and - adrenergic )
0.05 – 1.0 Dose related response, higher doses cause vasoconstriction. Useful in maintaining CO and BP inpatients unresponsive to dopamine or debutamine
Isoproterenol( - adrenergic )
0.05 – 0.5 Indicated in bradycardia unresponsive to atropine if increase in heart rate is not excessive, may be helpful in reactive pulmonary hypertension
Dopamine( - and -dopaminergic )
1 – 20 Cardiovascular effects are complex and dose related. Low dose infusion can restore cardiovascular stability and improve renal function
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Commonly Used Cardiovascular …(lanjutan)
Drug Dose (
ug/kg/min )
Comment
Dobutamine( - and - adrenergic )
1 – 20 Positive inotropic effect with minimal changes in heart rate or systemic vascular resistance
Amrinone 1 – 10 Initial bolus infusion may be required. Limited data available in children
VasodilatorsNitroprusside 0.005 – 8 Balanced arterial and venous
dilator. May result in thiocyanate or cyanide toxicity
Phentolamine 1 – 20 Causes dilatation of arterial and venus beds. Indirect inotropic effect may cause compensatory tachycardia
Nitroglicerine 0.5 – 20 Venus dilator. Dose not well established for infants and children
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MONITORING• State of Consiousness-Glasgow Coma Scale• Respiratory Rate and Character• Cardiovascular Parameters :
a. Skin and Core Temperature Differenceb. Pulse Rate and Volumec. Blood Pressured. Capillary Perfusion Timee. Central Venous Pressure Should Be Monitored in Patient Where There Has Been Poor Response To Fluid Therapy Or With Established Shock
• Urinary Output-Urine Bag, Or Preferably Catheter; Output Should Be 1-2 ml/kg Body Weight
• Pulse Oximetry• SvcO2
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KEY POINTS IN MANAGEMENT
Remember BP and pulse are unreliable indicators in early septic shock
Look for minor degrees of mental impairment (anxiety,restlessness)
Do not delay treatment, try to prevent the onset of hypotension, metabolic acidosis, and hypoxia
Give adequate fluids early in treatment, especially colloids
Do not use inotropic agents until the patients has received adequate fluid therapy
Monitor blood glucose, gases, and PH, and treat appropriately
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RINGKASAN/KESIMPULAN• Syok merupakan keadaan gawat darurat, sering
ditemukan pada anak• Morbiditas dan mortalitas syok masih tinggi• Syok hipovolemik, paling sering terjadi pada anak
(80%), sisanya syok kardiogenik• Diagnosis syok dini sulit, tetapi penting diketahui
melalui pemahaman patofisiologi syok (stadium kompensasi, dekompensasi dan ireversibel)
• Pengelolaan syok bertujuan meningkatkan DO2 melalui pe CO yaitu : 1. Memperbaiki prabeban dengan resusitasi volume2. Me kontraktilitas jantung dan 3. Me SVR
• Dengan pemahaman patofisiologi, diagnosis dini dan memperhatikan “key management“ syok, diharapkan dapat me mortalitas syok