syok hipovolemik [dr. erfan]
DESCRIPTION
hipovolemikTRANSCRIPT
1
Penderita wanita 22 th, Penderita wanita 22 th, ++ 70 kg masuk IRD 70 kg masuk IRD karena kecelakaan sepeda motor. Patah tulang karena kecelakaan sepeda motor. Patah tulang paha terbuka dan ada jejas di abdomen.Wanita paha terbuka dan ada jejas di abdomen.Wanita tersebut juga hamil 8 bulan, keluar perdarahan tersebut juga hamil 8 bulan, keluar perdarahan pervaginam. Nafas 36x/mnt, nadi 128 x/mnt, pervaginam. Nafas 36x/mnt, nadi 128 x/mnt, tensi 70/50. Tangan pucat dan dingin, hanya tensi 70/50. Tangan pucat dan dingin, hanya
ada respon dengan stimulasi nyeri. Dilaporkan ada respon dengan stimulasi nyeri. Dilaporkan oleh petugas ambulan 118, keadaan sekarang oleh petugas ambulan 118, keadaan sekarang ini seperti waktu di TKP. Selama perjalanan ke ini seperti waktu di TKP. Selama perjalanan ke IRD, di ambulan diberikan Ringer Lactate 2 liter IRD, di ambulan diberikan Ringer Lactate 2 liter
cepat, tensi pernah naik 90/60 dan nadi cepat, tensi pernah naik 90/60 dan nadi 120x/mnt120x/mnt Apakah penderita shockApakah penderita shock
Macam shock, penyebab, & Macam shock, penyebab, & patofisiologinyapatofisiologinya
Klasifikasi derajat shockKlasifikasi derajat shock Bagaimana tindakan pertolongan Bagaimana tindakan pertolongan
awalawal Bagaimana respon thd pemberian Bagaimana respon thd pemberian
cairancairan Bagaimana monitoringnya dan Bagaimana monitoringnya dan
evaluasinyaevaluasinya
??
2
SHOCKSHOCK
Inadequate organ perfusion and tissue Inadequate organ perfusion and tissue oxygenationoxygenation
3
BEBERAPA PERTANYAAN PENTING
1. SUDAH “ BERAPA LAMA” PENGERTIAN SYOK DIKENAL DIDUNIA KEDOKTERAN
2. APA MANFAAT MEMPELAJARI PARADIGMA SYOK, PADA SYOK KARENA PERDARAHAN
3. BAGAIMANA PARADIGMA PENGERTIAN SYOK PADA WAKTU INI
4. BAGAIMANA PARADIGMA PENANGGULANGAN SYOK PADA WAKTU INI
5. PELAJARAN FUNDAMENTAL APA YANG DAPAT DITARIK (LESSON LEARNED) DARI PERKEMBANGAN PARADIGMA SYOK TERSEBUT
4
PENGERTIAN SYOK SUDAH BERUMUR
LEBIH DARI 100 (SERATUS) TAHUN
AKHIR TAHUN 1800 AN – TAHUN 2000
5
• ADANYA SILENT EPIDEMIC KECELAKAAN LALU LINTAS• LANDASAN DOKTRIN TIME SAVING IS LIFE SAVING (WAKTU ADALAH NYAWA)• PARADIGMA GLOBAL PENANGGULANGAN SYOK PENDEKATAN SISTIM, FUNGSI, TERPADU DAN KOMPREHENSIF
• PARADIGMA GANGGUAN UTAMA PADA SYOK ADALAH GANGGUAN PERFUSI DAN GANGGUAN PENGGUNAAN OKSIGEN PADA JARINGAN ATAU SEL• SYOK KARENA PERDARAHAN (DALAM BATAS TERTENTU) DAPAT DIATASI DENGAN HEMODILUSI / TERAPI CAIRAN• MULAI DIKENAL PARU2 SEBAGAI TARGET ORGAN PADA SYOK - SHOCK LUNG, DANANG LUNG, ARDS
• PENGGUNAAN TRANSFUSI DARAH SECARA LUAS• MULAI DIKENALKAN DEXTRAN• PARADIGMA
-SYOK KARENA PERDARAHAN HARUS DIGANTI DENGAN DARAH
• TRANSFUSI DARAH MULAI DIPERGUNAKAN• PARADIGMA : SYOK KARENA HIPOTENSI• PENGGUNAAN VASOPRESOR
• SHOCK IS A RUDE UNHINGING OF THE MACHINERY OF LIFE• “SHOCK IS THE HARBINGER OF DEATH”
1980 AN - 2000
1957-1975PERANGVIETNAM
1950-1953PERANGKOREA
1939-1945PERANGDUNIA II
1914-1918PERANGDUNIA I
AKHIR TAHUN1800 AN
6
GARIS BESAR PERKEMBANGAN PARADIGMA PADA SYOK
1. SYOK DISEBABKAN OLEH KARENA HIPOTENSI
2. SYOK KARENA PERDARAHAN HARUS DIGANTI DENGAN DARAH
3. PADA SYOK GANGGUAN UTAMA ATAU GANGGUAN DASAR ADALAH GANGGUAN PADA PERFUSI DAN OKSIGENASI JARINGAN ATAU SEL MODEL DASAR PATHOFISIOLOGI SYOK
4. PADA SYOK KARENA PERDARAHAN PERBAIKAN PERFUSI DAN OKSIGENASI JARINGAN DAPAT DILAKUKAN DENGAN HEMODILUSI ATAU TERAPI CAIRAN
5. PARADIGMA GLOBAL MUTAKHIR PENGELOLAAN SYOK (PENGELOLAAN GAWAT DARURAT) PENDEKATAN SISTIM, FUNGSI, TERPADU DAN KOMPREHENSIV
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1. PARADIGMA : SYOK DISEBABKAN KARENA HIPOTENSI
ANGGAPAN DASAR :SYOK DISEBAKAN OLEH KARENA HIPOTENSI
ARAH TINDAKANDIBERIKAN VASOPRESOR
PARADIGMA DITINGGALKAN KARENA- DI KLINIK ANGKA KEHIDUPAN (SURVIVAL) TIDAK MENJADI BAIK
- PERCOBAAN BINATANG*. PEMBERIAN VASOPRESOR MALAH MEMPERTINGGI ANGKA KEMATIAN*. PADA SYOK SUDAH TERJADI PENINGKATAN KATEKOLAMIN (VASOPRESOR) ENDOGENUS
8
3. PARADIGMA : PADA SYOK GANGGUAN UTAMA ATAU GANGGUAN DASAR ADALAH GANGGUAN PADA PERFUSI DAN OKSIGENASI JARINGAN ATAU SEL
PENELITIAN KLINIK (PASIEN) ANGKA KEMATIAN SYOKBERKORELASI POSITIV DENGAN EKSES LAKTAT ATAULACTIC ACIDOSIS (1964)
LANDASAN PEMIKIRANPADA SITUASI NORMAL CUKUP PERFUSI ATAU OKSIGENASI METABOLISME AEROBIK GLUKOSA + O2 H2O + CO2 + 38 ATPPADA SYOK GANGGUAN PERFUSI ATAU OKSIGENASI METABOLISME ANAEROBIK GLUKOSA (TANPA O2) ASAM LAKTAT + 2 ATP
ARAH TINDAKANBAGAIMANA MEMPERBAIKI PERFUSI / OKSIGENASIJARINGAN SECEPATNYA
DOKTRIN TIME SAVING IS LIFE SAVING
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NUMBER OF PATIENTS = 43
10 14 20 13 6100
80
60
40
20
<13 13-40 41-80 81-120 >120
INITIAL ARTERIAL LACTATE mgm %
Arterial blood lactate determinations in 63 patients in shock, measuredWhen the patients were initially seen and before treatment was begunThis value was of prognostic, whereas a similar plot of initial bloodPreassure vs. Mortality was not
% M
OR
TA
LIT
Y R
AT
E
10
THE PATIENTS IN SHOCK
160
140
120
100
80
60
40
20
7.1 7.2 7.3 7,4 7,5 7,6
DIED
SURVIVED
ARTERIAL pH
LAC
TA
TE
mgm
%
A summary of 32 in whom serial measurements of arterial blood lactatereflect prognosis. In patents (represented by the broken lines) the lactaterose and all patients died. In 22 patients (respresented by the solid lines)the lactate dropped quickly to normal and all survived
+
++ + +
+ +
Bagan 4
11
100
80
60
40
20
00 30 60 90
Minutes
Percentsurvival
Golden hour. Probability of survival from posttraumatic shock
From: Stene JK, Grande CM, Gieseke A, 1991
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UNSUR2 PEMBEDA PADA SHOCK UNSUR YANGSAMA PADA SYOK
SYOK SYOK SYOK SYOK - COMMON HIPOVOLEMIA KARDIOGENIK ANAFILACTIC SEPTIK TERMINAL - PERDARAHAN PATH WAY - KEHILANGAN CAIRAN
GANGGUAN PENURUNAN PENURUNAN VASODILATASI GANGGUAN GANGGUAN PADA UTAMA VOLUME` DAYA POMPA PERFUSI &
DARAH JANTUNG OKSIGENASI
MEKANISME VOLUME DAYA POMPA PEMBULUH PERFUSI & FISIOLOGI DARAH JANTUNG DARAH OKSIGENASI DASAR JARINGAN /
SEL
ARAH UTAMA PENGGAN- PENINGKATAN PENGEMBALIAN PERBAIKAN PENGELO TIAN DAYA POMPA TONUS PEMBU - PERFUSI / LAAN VOLUME JANTUNG LUH DARAH OKSIGENASI
OBAT2 : OBAT2
- INOTROPIK VASO AKTIF - ANTI ARITMIK
Bagan 6
13
PERTOLONGAN PADA SYOK PENDEKATAN TERPADUBERORIENTASI FUNGSI / SISTIM
1. TAHAP PERTAMA / TAHAP SEGERA BERIKAN LIFE SUPPORT (BANTUAN HIDUP, RESUSITASI – STABILISASI)
PARU
AIRWAY CIRCULATION (A) BREATHING (C)
(B) BRAIN2. TAHAP KEDUA TETAPKAN DIAGNOSA DAN TERAPI DEFENITIF
JANTUNGO2
Bagan 9
14
4. PARADIGMA : PADA SYOK KARENA PERDARAHAN PERFUSI DAN OKSIGENASI JARINGAN DAPAT DIPERBAIKI DENGAN TERAPI CAIRAN (HEMODILUSI) UNTUK MENGEMBALIKAN VOLUME DARAH DAN MENINGKATKAN CARDIAC OUTPUT (1964)
KONSEP TERSEBUT DIGUNAKAN DENGAN LUAS PADAPERANG VIETNAM (1957 – 1975)
TEMUAN PADA PENELITIAN (BAIK PADA BINATANG MAUPUN PADA MANUSIA)PADA PERDARAHAN TERJADI 3 TAHAP PENYEMBUHAN :1. TAHAP VASOKONSTRIKSI - REDISTRIBUSI PROTEKTIV2. TAHAP HEMODILUSI3. TAHAP PRODUKSI ERITROSIT
PERBAIKAN PERFUSI DAN OKSIGENASI JARINGAN DAPATDILAKUKAN DENGAN TERAPI CAIRAN / HEMODILUSIUNTUK MEMPERCEPAT TAHAP HEMODILUSI
15
PERANG VIETNAM (1957 – 1975)
PERANG PALING LAMA UNTUK AMERIKA
MENINGGALORANG AMERIKA : 58.000VIETNAM UTARA : 500.000 – 1.000.000
LUKAAMERIKA : 365.000
BERATNYA PERANGBOM YANG DIJATUHKAN+ 4 X BOM DI JERMAN PADA PERANG DUNIA II
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LANDASAN PEMIKIRAN HEMODILUSI ATAU TERAPI CAIRAN
OKSIGEN = CARDIAC OUTPUT X SATURASI Hb% X Hb % X 1,34TERSEDIA (1) (2) (3)
FUNGSI FUNGSI FUNGSI SIRKULASI PERNAFASAN DAYA ANGKUT
OKSIGEN(RUMUS DARI NUNN)
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PENGGUNAAN = CARDIAC X ISI O2 ISI O2 OKSIGEN OUTPUT DARAH DARAH
ARTERI VENA
DALAM KEADAAN NORMAL Hb 15 G %
PENGGUNAAN O2 250 ml/mnt = 5000 X (20 ml/100 – 15 ml/100)DALAM KEADAAN HEMODILUSISETELAH PERDARAHANMISAL Hb 7,5 G % (50% HARGA NORMAL)
PENGGUNAAN O2 250 ml/me = (2X5000)X(10ml/100 – 7,5 ml/100)ISI O2 DARAH ARTERI TINGGAL 50% 10 ml/100ISI O2 DARAH VENA 7,5 ml/100PENGGUNAAN O2 PER 100 ml DARAH 2,5 ml/100PENGGUNAAN O2 DAPAT TETAPDIPERTAHANKAN 250 ml/me DENGAN MENAIKKANCARDIAC OUPUT 2 X MENJADI 10000 ml/me
KENAIKAN CARDIAC OUTPUT, DIMUNGKINKAN APABILA VOLUMEDARAH KEMBALI NORMAL DENGAN TERAPI CAIRAN
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5. PARADIGMA GLOBAL DALAM PENGELOLAAN SYOK (GAWAT DARURAT) PADA WAKTU INI
5.1. PENDEKATAN SISTIM SYOK (GD) DAPAT TERJADI PADA SIAPA
SAJA KAPAN SAJA, DIMANA SAJA
5.2. PENDEKATAN FUNGSITINDAKAN AWALLIFE SUPPORT (RESUSITASI STABILISASI)AIRWAY,M BREATHING, CIRCULATION, BRAINTINDAKAN BERIKUT:
DIAGNOSA DAN TERAPI DEFENITIV
5.3. PENDEKATAN TERPADUSYOK (GD) ADALAH MASALAH KOMPLEKSTERPADU DALAM SISTIM RUJUKANTERPADU DALAM TEAM MULTIDISIPLIN, MULTIPROFESI, MULTI SEKTOR
5.4. PENDEKATAN KOMPREHENSIVPRIMARY, SECONDARY DAN TERTIARY PREVENTION
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PENCEGAHAN PENANGGULANGANMULTI DISIPLIN
ANTARA LAIN SUMBER DAYA MANUSIA MULTI PROFESI- HELM YANG MEMBERI PERTOLONGAN MULTI SEKTOR- SABUK AWAM UMUM PETUGAS DOKTER PENGAMAN AWAM KHUSUS AMBULANS PERAWAT
TUJUAN MENCEGAH
MASYARAKAT KOMUNIKASI - KEMATIANAMAN / - KECACADANSEJAHTERA(SAFE COMMUNITY)
PASIEN AMBULANS PUSKESMAS RS.KLAS C RS. KLAS A/B
PRA RS INTRA RS INTRA RS
ANTAR RSPENDANAAN
TIME SAVING IS LIFE SAVING RESPONSE TIME DIUPAYAKAN SEPENDEK MUNGKIN MERUJUK THE RIGHT PATIENT, TO THE RIGHT PLACE AT THE RIGHT TIME
SPGDT-S (Sistim Pelayanan Gawat Darurat Terpadu-Sehari2)
TRANSPORTASI
+
20
SDM
5 DOKTER SPESIALIS : DIAGNOSA DEFENITIFTERAPI DEFENITIF
4. DOKTER UMUM : PPGD UNTUK DOKTER(PPGD - PENYELAMAT JIWA- LIFE SAVING FIRST AID- RESUSITASI - STABILISASI)ISI IDEAL PPGDBASIC LIFE SUPPORT ORIENTASIADVANCE LIFE SUPPORT UMUM
ADVANCE TRAUMA ORIENTASILIFE SUPPORT TRAUMA
ADVANCE CARDIAC ORIENTASILIFE SUPPORT JANTUNG
PEDIATRIC LIFE SUPPORTNEONATAL LIFE SUPPORT
DOKTER UMUM SEBAGAI : PELAKSANAMANAJER / KOORDINATOR PELATIH
3. PERAWAT : PPGD UNTUK PERAWAT
2. AWAM KHUSUS : PPGD UNTUK AWAM KHUSUSPOLISI, PEMADAM KEBAKARANPRAMUKA, PMI, HANSIP
1. AWAM UMUM : PPGD UNTUK AWAM UMUM 16Bagan 8
21
PERTOLONGAN PADA SYOK PENDEKATAN TERPADUBERORIENTASI FUNGSI / SISTIM
1. TAHAP PERTAMA / TAHAP SEGERA BERIKAN LIFE SUPPORT (BANTUAN HIDUP, RESUSITASI – STABILISASI)
PARU
AIRWAY CIRCULATION (A) BREATHING (C)
(B) BRAIN2. TAHAP KEDUA TETAPKAN DIAGNOSA DAN TERAPI DEFENITIF
JANTUNGO2
Bagan 9
22
MODEL PENDEKATAN TERPADU BERORIENTASI SISTIM / FUNGSI
PENYEBAB
PERDARAHANPOST PARTUM GANGGUAN
SISTIM / FUNGSI OBGINPECAHNYAVARICESS EVOPHAGUS SYOK PERTAMA KEDUA PENY.
KARENA LIFE SUPPORT DIAGNOSA DALAMFRAKTUR FEMUR PERDA - DANTERBUKA RAHAN PENGGANTIAN TERAPI BEDAH
VOLUME DEFENITIV
ORIENTASI FUNGSI /SISTIM
Bagan 10
50
40
30
20
10
0 0 1 2 3 4hr 1,2 5,6 weeks
Time ofter injury
Trimodal distribution of deaths (from Trankey DD:Sci Am 249 : 28: 35, 1983)
IMMEDIATE : CNS injury or heartand great vessel injury
EARLY : Major hemorrhage
LATE : Infection andmultiorgan failure
Pe
rce
nt o
f tra
um
a d
eat
hs
Bagan 12
24
PRIMARY CARAPREVENTION TERBAIK
HILANGKAN RESIKO
PENDEKATANKOMPREHENSIV SECONDARY CARA KEDUA PADA SHOCK PREVENTION TERBAIK
DIAGNOSA & TERAPI DINI
TERTIARY CARAPREVENTION TERAKHIR LIMIT THE DAMAGE
Bagan 13
25
Kontroversi Terakhir 2004
Syok karena perdarahan
1. Penggantian volume- Kristaloid
EBM tak ada beda- Koloid
- Plasma (?) cost – effective consideration
2. Penggunaan vasopresor- Sebagai terapi primer- Sebagai terapi penunjang untuk mencapai MAP optimal
26
……..Kontroversi terakhir 2004
3. Vasopresor yang mana- Dopamine
Beda atau sama- Norepinephrine - Indikasi utama bila ada unsur
vasodilatasi
4. RasionalTerapi utama volume replacementTerapi penunjang vasopresor
Catatan : Bila utamannya ada vasodilatasi Tujuan : MAP optimal Vasopresor yang berlebihan dapat berbahaya
27
Hershey / Lillehei (1964)
28
29
TachycardiaTachycardia VasoconstrictionVasoconstriction Cardiac Out PutCardiac Out Put Narrow Pulse PressureNarrow Pulse Pressure MAPMAP Blood FlowBlood Flow
RECOGNITION OF SHOCK STATERECOGNITION OF SHOCK STATERECOGNITION OF SHOCK STATERECOGNITION OF SHOCK STATE
Caution : Compensatory MechanismCaution : Compensatory Mechanism
30
31
Extremes of ageExtremes of age
AthletesAthletes
PregnancyPregnancy
MedicationsMedications
Hematocrit / hemoglobin concentrationHematocrit / hemoglobin concentration
PITFALL IN SHOCK RECOGNITIONPITFALL IN SHOCK RECOGNITIONPITFALL IN SHOCK RECOGNITIONPITFALL IN SHOCK RECOGNITION
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Liters
1
Saline Whole Blood
Resuscitation
Acute Hemorrhage
2
3
4
5
1 hour later
Cells
Plasma
HCT : 45%
HCT : 45%
HCT : 45%HCT : 27%
33
ICFICF
ISFISF
IVFIVF
ICFICF
ISFISF IVFIVF
Perdarahan
34
ICFICF
ICFICF
Perdarahan
ECF SHIFT
ISFISF
IVFIVF
ISFISF
IVFIVF
Squesterasi
35
Stage IStage I : vasoconstriction: vasoconstriction
Stage IIStage II II aII a : Transcapillary refill ISF : Transcapillary refill ISF IVF IVF
II b : Activation Renin–angiotensin– II b : Activation Renin–angiotensin– aldosteronaldosteron
Sodium + water retensionSodium + water retension
Stage IIIStage III : Erythrocyte production: Erythrocyte production
MILD HEMORRHAGEMILD HEMORRHAGE(<15% BV)(<15% BV)
MILD HEMORRHAGEMILD HEMORRHAGE(<15% BV)(<15% BV)
36
CELLULAR / METABOLIC RESPONSECELLULAR / METABOLIC RESPONSECELLULAR / METABOLIC RESPONSECELLULAR / METABOLIC RESPONSEBlood Loss
InadequatePerfusion
Further volume alteration
Fluid disturbance change
Membrane changes
Cell injury
Anaerobic metabolism
Organ dysfunction
Further circulation changes
Lactic acid Î
37
Most common Most common
Loss of circulating blood volumeLoss of circulating blood volume
Normal blood volume:Normal blood volume: Adult : 6-7% of ideal weight Adult : 6-7% of ideal weight
Child : 8-9% of ideal weightChild : 8-9% of ideal weight
HEMORRHAGIC SHOCKHEMORRHAGIC SHOCKHEMORRHAGIC SHOCKHEMORRHAGIC SHOCK
38
ASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENT
Airway and Breathing:Airway and Breathing:Oxygenate and ventilateOxygenate and ventilate
PaOPaO22 > 80 mmHg > 80 mmHg
SaOSaO22 > 95% > 95%
CirculationCirculationAssess (Class I, II, III, IV)Assess (Class I, II, III, IV)
Control HaemorrhageControl Haemorrhage
Prompt TreatmentPrompt Treatment
39
ASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENT
Disability – cerebral perfusionDisability – cerebral perfusion
Exposure / EnvironmentExposure / EnvironmentAssociated injuriesAssociated injuries
Prevent hypothermiaPrevent hypothermia
Gastric and bladder decompressionGastric and bladder decompression
Urinary outputUrinary output
40
Class I – IVClass I – IV
Not absoluteNot absolute
Only a clinical guideOnly a clinical guide
Subsequent treatment determined by Subsequent treatment determined by patient patient
responseresponse
CLASSIFICATION OF HEMORRHAGECLASSIFICATION OF HEMORRHAGECLASSIFICATION OF HEMORRHAGECLASSIFICATION OF HEMORRHAGE
41
CLASS I CLASS II CLASS III CLASS IV
Blood Loss (mL) Up to 750 750 – 1500 1500 – 2000 > 2000
Blood Loss (% Blood Vol)
Up to 15% 15 – 30 % 30 – 40 % > 40 %
Pulse Rate < 100 > 100 > 120 > 140
Blood Pressure Normal Normal
Pulse Pressure Normal or
Respiratory Rate 14 – 20 20 – 30 30 – 40 > 35
Urinary Output (ml/hr)
> 30 20 – 30 5 – 15 Negligible
CNS / Mental StatusSlightly anxious
Mildly anxiousAnxious, confused
Confiused, lethargic
Fluid Replacement (3:1 Rule)
Crystalloid CrystalloidCrystalloid and
bloodCrystalloid and
blood
Table 1. ESTIMATED FLUID AND BLOOD LOSSES Table 1. ESTIMATED FLUID AND BLOOD LOSSES *)*) Based on Patient’s Initial PresentationBased on Patient’s Initial Presentation
(For a 70 kg man)(For a 70 kg man)
Table 1. ESTIMATED FLUID AND BLOOD LOSSES Table 1. ESTIMATED FLUID AND BLOOD LOSSES *)*) Based on Patient’s Initial PresentationBased on Patient’s Initial Presentation
(For a 70 kg man)(For a 70 kg man)
42
MANAGEMENT VASCULAR ACCESSMANAGEMENT VASCULAR ACCESSMANAGEMENT VASCULAR ACCESSMANAGEMENT VASCULAR ACCESS
2 large-caliber peripheral IV’s2 large-caliber peripheral IV’s
Central accessCentral accessFemoralFemoral
JugularJugular
SubclavianSubclavian
IntraosseousIntraosseous
Obtain blood for crossmatchObtain blood for crossmatch
43
Flow rate(mL/min)
200
100
14 ga
Short Catheter
Short Catheter
16 ga 16 ga 16 ga
2 in 2 in 5,5 in 12 in
Diameter
Length
44
45
MANAGEMENT FLUID THERAPYMANAGEMENT FLUID THERAPYMANAGEMENT FLUID THERAPYMANAGEMENT FLUID THERAPY
Warmed Warmed crystalloid solutioncrystalloid solution
Rapid fluid bolusRapid fluid bolusAdult : 2 liters Ringer’s LactateAdult : 2 liters Ringer’s Lactate
Child : 20 ml/kg Ringer’s LactateChild : 20 ml/kg Ringer’s Lactate
Monitor response to initial therapyMonitor response to initial therapy
46
THERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSTHERAPEUTIC DECISIONS
Patient response determines subsequent Patient response determines subsequent therapytherapy
Hemodynamically Hemodynamically ‘normal’ ‘normal’ vs vs hemodinamically hemodinamically ‘‘
‘ ‘stable’stable’
Recognize need to resuscitate in operating Recognize need to resuscitate in operating roomroom
47
Rapid Response
Transient Response
No Response
Vital Signs Return to normalTransient improve-ment; recurrence of
BP and HRRemain abnormal
Estimated Blood loss
Minimal (10-20%)
Moderate and ongoing (20-40%)
Severe (>40%)
Need for more Crystalloid
Low High High
Need for Blood Low Moderate to high Immediate
Blood PreparationType and
crossmatchType – specific
Emergency blood release
Need for Operative Intervension
Possibly Likely Highly likely
Early Presence of Surgeon
Yes Yes Yes
Table 2. RESPONSES TO INITIAL FLUID Table 2. RESPONSES TO INITIAL FLUID RESUSCITATION RESUSCITATION *)*)
Table 2. RESPONSES TO INITIAL FLUID Table 2. RESPONSES TO INITIAL FLUID RESUSCITATION RESUSCITATION *)*)
*) 2000 ml RL solution in adults, 20 ml/Kg RL bolus in children over *) 2000 ml RL solution in adults, 20 ml/Kg RL bolus in children over 10-15 min10-15 min
48
VOLUME REPLACEMENTVOLUME REPLACEMENTVOLUME REPLACEMENTVOLUME REPLACEMENT
Warmed fluidsWarmed fluids
Crossmatch, PRBCCrossmatch, PRBC
Type-specificType-specific
Type O, Rh-negativeType O, Rh-negative
AutotransfusionAutotransfusion
CoagulopathyCoagulopathy
49
Flow rate(mL/min)
100
50
Water 5% Albumin
WholeBlood
PackedRBCs
Catheter Dimension16 gauge diameter2 inches in length
50
REEVALUATE ORGAN PERFUSIONREEVALUATE ORGAN PERFUSIONREEVALUATE ORGAN PERFUSIONREEVALUATE ORGAN PERFUSION
MONITOR : MONITOR : Vital signsVital signs CNS StatusCNS Status Skin perfusionSkin perfusion Urinary outputUrinary output Pulse oximetryPulse oximetry End Tidal CO2End Tidal CO2 Oxygen ExtractionOxygen Extraction Acid baseAcid base
51
RESUSCITATION / EVALUATIONRESUSCITATION / EVALUATIONRESUSCITATION / EVALUATIONRESUSCITATION / EVALUATION
Urinary output : Urinary output : Adults : 0,5 ml/kg/hourAdults : 0,5 ml/kg/hour Child : 1 ml/kg/hourChild : 1 ml/kg/hour Infant : 2 ml/kg/hourInfant : 2 ml/kg/hour Inadequate output suggests Inadequate output suggests
inadequate inadequate
resuscitationresuscitation
52
ET CO2
(mmHg)
30
10
20
1 2 3 4 5
Volume Infused (Liters)
53
SaO2 SvO2 SaO2 – SvO2
Normal > 95% > 65% 20 – 30 %
Hypovolemia > 95% 50 – 65 % 30 – 50 %
Hypovolemic shock
> 95% < 50 % > 50 %
54
AVOIDING COMPLICATIONAVOIDING COMPLICATIONAVOIDING COMPLICATIONAVOIDING COMPLICATION
Fluid overloadFluid overload
Invasive monitoring (ICU) Invasive monitoring (ICU) CVPCVP
Pulmonary artery catheterPulmonary artery catheter
Other problems :Other problems :Resuscitation induced haemorrhageResuscitation induced haemorrhage
Post resuscitation injuryPost resuscitation injury
No – Reflow phenomenonNo – Reflow phenomenon
Reperfusion injuryReperfusion injury
55
CVP CATHETERCVP CATHETERCVP CATHETERCVP CATHETER
Catheter in Right atriumCatheter in Right atrium
Via : Via : Vena cubitiVena cubiti
Vena subclaviaVena subclavia
Vena jugularis internaVena jugularis interna
Vena femoralisVena femoralis
56
CVP CVP MONITORINGMONITORINGCVP CVP MONITORINGMONITORING
Monitors right heart’s ability to accept Monitors right heart’s ability to accept
fluid loadfluid load
CVP level vs actual blood volumeCVP level vs actual blood volume
Low / declining : Replace fluidsLow / declining : Replace fluids
Elevated : adequate fluids, Elevated : adequate fluids,
hypervolemia, cardiothoracic problemhypervolemia, cardiothoracic problem
Elective, monitoring lineElective, monitoring line
57
58
59
60
RL 50 cc/10 mnt RL 100 cc/10 mnt
FLUID CHALLENGE TESTFLUID CHALLENGE TEST( Rule 2 – 5 )( Rule 2 – 5 )
FLUID CHALLENGE TESTFLUID CHALLENGE TEST( Rule 2 – 5 )( Rule 2 – 5 )
C V P
RL 200 cc/10 mnt
< 8 cm H2O 8-14 cm H2O > 14 cm H2O
Kenaikan C V P
Ulang
< 2 cm H2O
Tunggu 10 menit
2-5 cm H2O
STOP
> 5 cm H2O
< 2 cm H2O 2-5 cm H2O
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Recoqnize inadequate organ perfusion and Recoqnize inadequate organ perfusion and
oxygenationoxygenation
Identify the cause :Identify the cause :HaemorrhageHaemorrhage
Non haemorrhageNon haemorrhage
TreatmentTreatmentStop the cause / bleedingStop the cause / bleeding
Restore volume and perfusionRestore volume and perfusion
SHOCK MANAGEMENTSHOCK MANAGEMENTSHOCK MANAGEMENTSHOCK MANAGEMENT
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40 %40 %
ICFICF
KK
15 %15 %
ISFISF
NaNa
5% 5%
IVFIVF
NaNa
ICFICF
ISFISF
IVFIVF
ICFICF
ISFISF
IVFIVF
ICFICF
ISFISF
IVFIVF
D 5 % Koloid
RL / NS
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ICFICF
ISFISF
IVFIVF
NonPerdarahan
ICFICF
ISFISF
IVFIVF
ICFICF
ISFISF
IVFIVF
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Recognize shockRecognize shock
Stop the bleeding !Stop the bleeding !
Resplenish intravascular Resplenish intravascular volumevolume
Restore organ perfussionRestore organ perfussion
ASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENTASSESSMENT & MANAGEMENT
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THERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSRapid ResponseRapid Response
THERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSRapid ResponseRapid Response
< 20% blood loss < 20% blood loss
Responds to fluid replacementResponds to fluid replacement
Surgical consultation, evaluationSurgical consultation, evaluation
Continue to monitorContinue to monitor
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THERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSTransient ResponseTransient Response
THERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSTransient ResponseTransient Response
20% - 40% blood loss20% - 40% blood loss
Deteriorates after initial fluodsDeteriorates after initial fluods
Surgical consultation, evaluationSurgical consultation, evaluation
Continued fluids plus bloodContinued fluids plus blood
Continued hemorrhage OperationContinued hemorrhage Operation
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THERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSMinimal to No ResponseMinimal to No ResponseTHERAPEUTIC DECISIONSTHERAPEUTIC DECISIONSMinimal to No ResponseMinimal to No Response
>40% blood loss>40% blood loss
No response to fluid resuscitationNo response to fluid resuscitation
Immediate surgical consultationImmediate surgical consultation
Exclude non hemorrhagic shockExclude non hemorrhagic shock
Immediate operationImmediate operation
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