syok hipovolemik [dr. erfan]

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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

7

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

9

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

12

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

16

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)

17

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

18

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

19

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

32

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

64

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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