DEFINISI

Suatu sindrome klinik yang mempunyai ciri-ciri

dapat berupa
• Hipotensi, Takikardi, Takipneu, Kulit yang dingin, Pucat
basah, Sianosis perifer,Perubahan status mental dan
Penurunan pembentukan urine .

Suatu keadaan yang terjadi bila perfusi oksigen

terganggu ke jaringan atau menjadi tidak adekuat
 KLASIFIKASI SYOK

• Hypovolemic Shock
–blood VOLUME problem
• Cardiogenic Shock
–blood PUMP problem
• Distributive Shock
[septic;anaphylactic;neurogenic]
–blood VESSEL problem
WHAT DID GUYTON TEACH US ?
WHAT DID GUYTON TEACH US ?
 CIRCULATION (VENOUS RETURN)
DETERMINES THE CARDIAC OUTPUT
• CARDIAC OUTPUT
• RETURN FUNCTION CARDIAC FUNCTION
• STROKE VOLUME X HR
CVP AFTERLOAD
CENTRAL
VENOUS PRELOAD
PRESSURE CONTRACTILITY
RVR
RESISTANCE TO VENOUS RETURN
DIAMETER VEIN CAVA AND BLOOD
VISCOSITY
THE HEART CANNOT PUMP
MCFP
MEAN SYSTEMIC FILLING PRESSURE OUT MORE VOLUME THAN
 STRESSED VOLUME (NON-
SPLANCHNIC CIRCULATION)
COMES BACK

Circulatory Physiology: Cardiac Output And Its Regulation. A.C.

Guyton.W.B. Saunders Co. Philadelphia 1963
60 % BB = AIR
 KOMPOSISI CAIRAN TUBUH

TUBUH MANUSIA TERDIRI DARI :

ZAT PADAT : 40 % BERAT BADAN
ZAT CAIR : 60 % BERAT BADAN

TOTAL CAIRAN TUBUH BERKISAR 55-70% BERAT BADAN

TERGANTUNG PADA
UMUR
JENIS KELAMIN
BILA SEORANG DGN BB 60Kg= 60 x 60% = 36 L
DISTRIBUSI CAIRAN TUBUH

CIS CISt CIV

DEKST.5%

40% 15% 5% RINGER

LAKTAT
NACL 0,9%

DARAH
KOLOID
PROT. PLASMA
KLASIFIKASI SYOK
1. Syok hipovolemik

2. Syok kardiogenik

3. Syok anafilaktik

4. Syok distributif  Syok septik

5. Syok neurogenic
 PENDAHULUAN

GANGGUAN CAIRAN &

ELEKTROLIT

KEGAWATAN

KEMATIAN
SEBAB UTAMA GANGGUAN CAIRAN DAN
ELEKTROLIT
ASUPAN YG KURANG
SUHU LINGKUNGAN YG TINGGI
PERDARAHAN BANYAK
DIARE
PUASA
MUNTAH-MUNTAH
PERITONITIS
ILEUS OBSTRUKSI
TERBAKAR
 PENGERTIAN SYOK HIPOVOLEMIK

ADALAH :
SYOK YANG DISEBABKAN OLEH
KEHILANGAN SEJUMLAH BESAR
CAIRAN TUBUH (EKSTRASELULER)
ETIOLOGI
SYOK HIPOVOLEMIK

PERDARAHAN BUKAN PERDARAHAN

(HIPOVOLEMI) (DEHIDRASI)
- PERDARAHAN - MUNTAH, DIARE
- PUASA YG LAMA
- BERADA DI T4 YG SGT
PANAS
- TERBAKAR
PERDARAHAN SYOK
HIPOVOLEMIK

KONSEKUENSI
SHOCK TIME METABOLIK

RESUSITASI
CAIRAN
 Patofisiologi Perdarahan
PERDARAHAN

KEHILANGAN VOLUME
(gangguan curah jantung & perfusi)
dan
KEHILANGAN HEMOGLOBIN
(gangguan oksigenasi jaringan)

TAKIKARDIA VASO TRANSCAPILLARY ERITRO SINTESA

KONSTRIKSI REFILL POESIS PROTEIN

DAPAT KOMPENSASI
KOMPENSASI CEPAT DIPERCEPAT LAMBAT
SUDAH MAKSIMAL
Mekanisme Kompensasi
Perdarahan
 Gejala Klinis & Estimasi Perdarahan

1. GEJALA KLINIK
ESTIMATED BLOOD LOSS
GEJALA
( EBV = 65-70 ML/KGBB )

10-15 % EBV Minimal

15-25 % EBV Pre syok, akral dingin

Syok, perfusi menurun

25-35 % EBV TS < 90, N > 120

Syok berat, perfusi sangat

buruk, tensi tak terukur, nadi
> 35-40 % EBV tak teraba, gangguan
kesadaran
2. TRAUMA STATUS DARI GIESECK
TANDA, TS I TS II TS III

Sesak nafas - Ringan ++

Tekanan darah N Turun Tak terukur

Nadi Cepat Sangat cepat Tak teraba

Urine N Oligouria Anuria

Kesadaran N Disorientasi / koma

Gas darah N pO2  /pCO2 pO2  /pCO2 

CVP N Rendah Sangat rendah

Blood loss % EBV Sampai 10 % Sampai 30 % Sampai 50 %

 3. PEDOMAN COMMITTEE ON TRAUMA ATLS 1989
Kelas I Kelas II Kelas III Kelas IV

Kehilangan darah (ml) Sampai 750 750-1500 1500-2000 > 2000

Kehilangan darah (%
Sampai 15 % 15-30 % 30-40 % > 40 %
volume darah)
Denyut nadi < 100 > 100 > 120 > 140

Tekanan darah Normal Normal Menurun Menurun

Tekanan nadi Normal atau naik Menurun Menurun Menurun

Frekuensi pernapasan 14-20 20-30 30-40 > 35

Produksi urine (ml/jam) > 30 20-30 5-15 Tidak berarti

Bingung, lesu
CNS / status mental Sedikit cemas Agak cemas Cemas, bingung (lethargic)

Kristaloid dan Kristaloid dan

Pengganti cairan (hukum 3:1) Kristaloid Kristaloid darah
darah
Untuk laki-laki yang beratnya 70 kg
 DEHIDRASI
GEJALA KEKURANGAN CES

TURGOR KULIT YG JELEK

MATA CEKUNG
UBUN-UBUN CEKUNG(PD BAYI & ANAK)
MUKOSA BIBIR DAN KORNEA KERING

BILA DIIKUTI GANGGUAN HEMODINAMIK

MAKA GEJALA-GEJALA YANG MUNCUL :

– HIPOTENSI
– TAKIKARDI
– VENA-VENA KOLAPS
– OLIGOURI
– SYOK
 GEJALA & DERAJAT DEHIDRASI
1. DEHIDRASI RINGAN (DEFISIT 4% BB)
- TURGOR KULIT SEDIKIT MENURUN
- TAKIKARDI
- HAUS
2. DEHIDRASI SEDANG (DEFISIT 8% BB)
- TURGOR KULIT JELAS MENURUN
- HIPOTENSI POSTURAL
- TAKIKARDI
- NADI LEMAH
- SANGAT HAUS
3. DEHIDRASI BERAT (DEFISIT 12% BB)
- TURGOR KULIT SGT MENURUN - STUPOR/KOMA
- HIPOTENSI - NADI HILANG
- SIANOSIS UJUNG JARI - SHOCK
 JENIS-JENIS DEHIDRASI
DAN PENYEBABNYA
1. DEHIDRASI ISOTONIS
ILEUS OBSTRUKSI
PERITONITIS
DIARE
BERKERINGAT BANYAK
2. DEHIDRASI HIPERTONIS
PANAS YG TINGGI
PUASA
POLIURI
HIPERELEMENTASI LAMA
3. DEHIDRASI HIPOTONIS
REHIDRASI DGN DEXTROSE 5% YG BLM CUKUP
GANGGUAN REABSORBSI Na
Pilihan Cairan
1. Cairan kristaloid
a) NaCl 0,9%
b) Ringer laktat
c) Ringer asetat
2. Cairan koloid
 Alami : plasma, albumin
 Buatan : gelatin, starch, dextran
3. Cairan hipertonik + Dextran
Teknik Resusitasi Cairan
PERDARAHAN
TENTUKAN DERAJAT PERDARAHAN
TEKNIK RESUSITASI
Pemberian kristaloid : 3 kali perdarahan
 Ringer laktat
 Ringer asetat
 NaCl 0,9 %
Cairan koloid : sesuai jumlah perdarahan
 Dextran
 Expafusin
 Hemacel
Darah : transfusi
DISTRIBUSI CAIRAN TUBUH

CIS CISt CIV

DEKST.5%

40% 15% 5% RINGER

LAKTAT
NACL 0,9%

DARAH
KOLOID
PROT. PLASMA
 DEHIDRASI

TENTUKAN JENIS DEHIDRASI

UNTUK PEMILIHAN CAIRAN RESUSITASI YG TEPAT
TENTUKAN DERAJAT DEHIDRASI
UNTUK MEMPERKIRAKAN DEFISIT
TEKNIK PEMBERIAN CAIRAN
SETENGAH DEFISIT (50%) DIBERIKAN DALAM 8 JAM PERTAMA,
50% SISA DIBERIKAN DALAM 16 JAM BERIKUTNYA.
AGAR GGN HEMODINAMIK CEPAT TERATASI, MAKA DLM 1 JAM
I DAPAT DIBERIKAN 20 – 40 ML/KG.BB
 ALGORITME RESUSITASI CAIRAN
PENDERITA SYOK HIPOVOLEMIK

PASANG INFUS JARUM BESAR CATAT TEKANAN DARAH,

AMBIL CONTOH DARAH
RINGER LAKTAT Atau NaCl 0,9 %
30 ml/KgBB dlm 30-60 MENIT,
(kalau perlu 2 infus)
NADI, PERFUSI, (produksi
urine)
(Siap darah 500-1000 ml Bila di
sebabkan perdarahan)

HEMODINAMIK BAIK HEMODINAMIK BURUK

TERUSKAN CAIRAN
(Diulang seperti diatas )
Tekanan darah > 100, nadi < 100
Perfusi hangat, kering
Urine > ½ ml / kg / jam
HEMODINAMIK BAIK HEMODINAMIK BURUK

A B C
A : INFUS DILAMBATKAN DAN BIASANYA
TRANSFUSI TDK DIPERLUKAN

B : JIKA Hb < 8 gr% ATAU HCT < 25%

SEBAIKNYA TRANSFUSI DIBERIKAN

C : TRANSFUSI HARUS SEGERA DIBERIKAN

( BIASANYA PADA SYOK BERAT DAN ANEMIA BERAT )
Monitoring
1. TEKANAN DARAH
2. NADI
3. URINE
4. PERFUSI (hangat, merah
kering)
5. C V P
6. SUHU
7. THORAKS FOTO
8. ECG
Kebutuhan dasar cairan rata-rata : 30-50 ml/KgBB/24jam

Kebutuhan dasar Na+ rata-rata : 2-3 mEq/KgBB/24jam

Kebutuhan dasar K+ rata-rata : 1-2 mEq/KgBB/24jam

 Water Demand per-day
Urine production (24 h) 1500 mL
Insensible loss 1.3 x 700 mL 900 mL
(Indonesian BSA = 1.3 m2)
Water with faeces 100 mL
Total 2500 mL

Water from body metabolism is 350/m2 BSA:

1.3 x 350 mL = 500 mL.

Minimal water demand in 24 hours:

2500 mL – 500 mL = 2000 mL (without febris)

…Or demand of water in 24 hours is 35 mL/kg.

A man 65 kg needs water as much as 65 x 35 mL = 2000 mL/24 h.

If febris is present, each 1C of body temp.  10-15% total demand
 Variasi berdasarkan* :
• Tonisitas
Kristaloid • Kandungan elektrolit
*Terhadap plasma
Air

Solut
sederhana

Kristaloid dapat
berupa Larutan ionik
Contoh: Ringer asetat/laktat, NS 0,9%, etc

Larutan non-ionik
Contoh : Dextrose 5%, Maltose 10%, etc
 Cairan • Asering ( Ringer asetat )
• Ringer laktat
kristaloid • Na Cl 0,9%

Cairan • Alami : plasma, albumin

koloid • Buatan : dextran L,gelatin, strach.

Cairan • D10%

hipertoik • Maltose 10%

 Perbandingan komposisi RL dan Asering

Osmolaritas
ELEKTROLIT (mEq/L)
Nama product
Na+ K+ Cl- Ca- Laktat- Acetat
- mOsm/L

RL (Ringer Laktat)
130 4 109 3 28 - 273

ASERING (Ringer Asetat)

130 4 109 3 - 28 273
 NaCl 0.9 % vs ASERING
Peningkatan terjadinya
asidosis metabolik hipercloremia
yg selama ini dianggap tdk
berdampak negatif & akan hilang dgn
sendirinya ternyata dpt mengganggu
perfusi organ akhir &
mekanisme pertukaran sel.

Dexter et al : berdampak negatif pd

RBF & GFR
 Sifat-sifat ekspander/substitut
plasma ideal
• Larutan stabil dan mudah disimpan utk waktu yang lama.
• Koloid bebas dari zat-zat pirogen, antigen dan toksik.
• TOK yang adekuat dicapai dengan waktu paruh beberapa
jam. TOK hendaknya dipertahankan di atas 2,7 kPa (20
mmHg) yaitu 70% TOK rata-rata normal 3,7 kPa (28 mmHg).
TOK 2,7 kPa (20 mmHg) dihasilkan oleh protein serum total
50 g / L.
• Metabolisme dan ekskresi koloid tidak menimbulkan efek
yang tak diinginkan pada resipien.
 Sifat-sifat ekspander/substitut
plasma ideal
• Infus tidak mengakibatkan koagulopati, hemolisis,
aglutinasi sel darah merah, atau gangguan cocok
silang.
• Mengganti kehilangan volume darah dengan cepat.
• Mengembalikan keseimbangan hemodinamik.
• Menormalkan aliran sirkulasi mikro.
• Memperbaiki hemoreologi.
• Memperbaiki penyediaan O2 dan fungsi organ.
Dekstran • Polisakarida rantai tunggal
• Berat molekul berkisar 10-90 kDa.
(Tersedia dalam sediaan : 40, 60 dan 70 kDa)
• Kekuatan onkotik tiap 1g terhadap air:
– Dekstran 40  30 mL
– Dekstran 70  20 mL
• Berada dalam intravaskuler selama :
– Dekstran 40  3-4 jam
– Dekstran 70  6-8 jam
E
Hemostasis : Pemanjangan waktu perdarahan (>1,5g/kg dekstran)
F • Berkurangnya faktor VIII
E • Berkurangnya faktor Von Willenbrand
K • Berkurangnya fibrin
Ginjal : gagal ginjal (oligouri-anuri) → sindrom hipertonik akut
Alergi : reaksi anafilaktik sering ditemukan
(dibanding substitusi plasma lainnya)
Dekstran
Karena efek samping yang merugikan dari dekstran
penggunaannya secara klinis sangat banyak berkurang
 Gelatin
• Product of BOVINE COLLAGEN
• Rata-rata berat molekulnya 35 kDa
– Mudah berpindah ke jaringan interstisiel
– Tidak terakumulasi dalam tubuh
– Berada dalam intravaskuler selama 3-4 jam

E
F
• Hemostasis
– Perubahan pada tromboelastogram
E
– Mengurangi kemampuan agregasi trombosit
K
• Alergi : insidens reaksi alergi lebih rendah dibandingkan
pada penggunaan dekstran.
Gelatin

Penggunaan gelatin secara klinis sebagai

ekspander volume plasma untuk perdarahan
akut.
HES (Hydroxy Ethyl Starch)
• Merupakan modifikasi dari kanji (starch) alami
• Starch alami mudah dihidrolisa oleh enzim amilase
• Hidroksietil digunakan untuk mensatbilkan larutan

Klasifikasi HES (in vitro) berdasarkan berat molekulnya :

High Mollecular Weight (HMW) → 450 kDa
Medium Mollecular Weight (MMW) → 200 kDa
Low Mollecular Weight (LMW) → 70 kDa
 Hydroxy Ethyl Starch

• Low MW:
– Expafusin 6%, (40,000 / 0.5 – 0.55) in balanced salt solution
– Voluven 6%, (130,000 / 0.4) in NaCl 0.9%

• Medium MW:
– Haes-steril 6%, 10% 200,000 / 0.5 in NaCl 0.9%
– Hemohes 6%, 200,000 / 0.5 in NaCl 0.9%
– Widahes 6%, 200,000 / 0.5 in NaCl 0.9%
– Fimahes 6%, 200,000 / 0.6 in balanced electrolyte sol

• High MW:
– HES (450,000 / 0.7)
HES
• Hemostasis
– Pemanjangan APTT
– Penurunan kadar : - Faktor VIII
- Faktor Von Willenbrand

Efek Samping
• Ginjal
– “Acute hyperoncotic kidney failure syndrome”
• Pemberian HMW-HES
• Pemberian berulang

• Alergi
– Baik sehubungan dengan toleransi imunologis
• Insidens reaksi alergi rendah dibanding dekstran dan gelatin
• Jarang menimbulkan reaksi yang berat
HES
 Albumin Dekstran Gelatin HES
Koloid 5% 20-25% 40 70 Gelatin Polygelin 6% 10%
Na+ 154 154 130 154 142 145 154 154
Elektrolit

K+ - - 4 - - 5.1 - -
Ca++ - - 3 - 80 145 - -
Cl- 154 154 109 154 1.4 6.25 154 154
Laktat - - 28 - - - - -
Asetat - + - - - - - -
BM (Kda) 69 69 40 70 30-35 30-35 100-450 100-450
Osmolalitas
300 1500 306 349 300-350 300-350 280-324 280-324
(mOsm/L)
Tek.Onkotik
19-30 74-120 20-60 20-60 70-100 70-100 23-82 23-82
(mmHg)
Ekspansi vol. (%) 70-100 200-300 100-200 80-140 70-100 70-100 100-160 100-160
Durasi (jam) <24 <24 <4-6 <8-24 <4-6 <4-6 <4-36 <4-36
t 1/2 (jam) 16-24 16-24 2 ~24 ~2-9 ~2-9 2-12 2-12
• Tidak dapat dengan mudah atau segera diperoleh
• Risiko penularan penyakit infeksi (HIV, Hepatitis)
• Merupakan koloid alami yang paling ideal namun efikasi secara
klinis tidak menunjukkan hal yang demikian.

• Tidak lebih efektif secara klinis dibandingkan koloid sintetik,

atau bahkan kristaloid dalam mengurangi tingkat mortalitas
• Mahal
 Shock Syndromes

• Hypovolemic Shock
–blood VOLUME problem
• Cardiogenic Shock
–blood PUMP problem
• Distributive Shock
[septic;anaphylactic;neurogenic]
–blood VESSEL problem
 Cardiogenic Shock
• The impaired ability of the
heart to pump blood
• Pump failure of the right
or left ventricle
• Most common cause is LV
MI (Anterior)
• Occurs when > 40% of
ventricular mass damage
• Mortality rate of 80 % or >
 Cardiogenic Shock:
Pathophysiology

• Impaired pumping ability of LV leads to…

+ Decreased stroke volume leads to…..
+ Decreased CO leads to …..
+ Decreased BP leads to…..
+ Compensatory mechanism which may lead to …
+ Decreased tissue perfusion !!!!
 Cardiogenic Shock: Clinical
Presentation
Abnormal heart sounds

• Murmurs
• Pathologic S3 (ventricular gallop)
• Pathologic S4 (atrial gallop)
 CLINICAL ASSESSMENT

• Pulmonary & • PaO2

Peripheral Edema • UOP
• CO • Hemodynamic changes:
• Hypotension PCWP,PAP,RAP & SVR
• Tachypnea,
 COLLABORATIVE MANAGEMENT

• Treatment is aimed at :
• Goal of management : • Early assessment &
• Treat Reversible Causes treatment!!!
• Protect ischemic • Optimizing pump by:
myocardium – Increasing myocardial O2
• Improve tissue perfusion delivery
– Maximizing CO
– Decreasing LV workload
(Afterload)
 COLLABORATIVE MANAGEMENT

Limiting/reducing myocardial damage during

Myocardial Infarction:
• Increased pumping action & decrease workload
of the heart
– Inotropic agents
– Vasoactive drugs
– Cautious administration of fluids
• Consider thrombolytics, angioplasty in specific cases
 Management Cardiogenic Shock

OPTIMIZING PUMP FUNCTION:

– Pulmonary artery monitoring is a necessity !!
– Aggressive airway management: Mechanical
Ventilation
– Judicious fluid management
– Vasoactive agents
• Dobutamine
Management Cardiogenic Shock

OPTIMIZING • Morphine as needed (Decreases preload, anxiety)

PUMP • Cautious use of diuretics in CHF
• Vasodilators as needed for afterload reduction
FUNCTION • Short acting beta blocker, esmolol, for refractory
tachycardia
(CONT.):

MONACO
 Distributive Shock

Perfusi oksigen tidak adekuat disebabkan

maldistribusi cairan tubuh

Volume Intravascular maldistribusi karena

terjadinya kelainan pada pembuluh darah vena

Pompa Jantung dan Volume Intravasculer

Normal tapi darah tidak sampai ke jaringan
 Vasogenic/Distributive Shock

• Etiologies
– Septic Shock (Most Common)
– Anaphylactic Shock
– Neurogenic Shock
 Anaphylactic Shock

• A type of distributive shock that results from

widespread systemic allergic reaction to an
antigen
• This hypersensitive reaction is LIFE
THREATENING
Pathophysiology Anaphylactic Shock

• Antigen exposure
• body stimulated to produce IgE antibodies specific
to antigen
– drugs, bites, contrast, blood, foods, vaccines

• Reexposure to antigen
– IgE binds to mast cells and basophils
• Anaphylactic response
 Anaphylactic Response

• Vasodilatation
• Increased vascular permeability
• Bronchoconstriction
• Increased mucus production
• Increased inflammatory mediators
recruitment to sites of antigen interaction
 Clinical Presentation
Anaphylactic Shock

Almost immediate response to inciting antigen

Cutaneous manifestations
• urticaria, erythema, pruritis, angioedema

Respiratory compromise
• stridor, wheezing, bronchorrhea, resp. distress

Circulatory collapse
• tachycardia, vasodilation, hypotension
 Management Anaphylactic Shock
• Early Recognition, treat aggressively
• AIRWAY SUPPORT
• IV EPINEPHRINE (open airways)
• Antihistamines, diphenhydramine 50 mg IV
• Corticosteroids
• IMMEDIATE WITHDRAWAL OF ANTIGEN IF
POSSIBLE
• PREVENTION
 Management Anaphylactic Shock

• Judicious crystalloid administration

• Vasopressors to maintain organ perfusion
• Positive inotropes
• Patient education
 NEUROGENIC SHOCK

• A type of distributive shock that results from the loss

or suppression of sympathetic tone
• Causes massive vasodilatation in the venous
vasculature,  venous return to heart,  cardiac
output.
• Most common etiology: Spinal cord injury above T6
• Neurogenic is the rarest form of shock!
Pathophysiology of Neurogenic Shock

Distruption of sympathetic nervous system

Loss of sympathetic tone

Venous and arterial vasodilation

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen supply

Impaired tissue perfusion

Impaired cellular metabolism

 Assessment, Diagnosis and Management of
Neurogenic Shock
PATIENT ASSESSMENT
• Hypotension MEDICAL MANAGEMENT
• Bradycardia • Goals of Therapy are to
treat or remove the cause
• Hypothermia
& prevent cardiovascular
• Warm, dry skin instability, & promote
• RAP  optimal tissue perfusion
• PAWP 
• CO 
• Flaccid paralysis below
level of the spinal lesion
 MANAGEMENT OF
NEUROGENIC SHOCK

Hypovolemia- tx with careful fluid replacement for

BP<90mmHg, UO<30cc/hr
Changes in LOC
Observe closely for fluid overload
Vasopressors may be needed
Hypothermia- warming txs
-avoid large swings in pts body temperature
Treat Hypoxia
Maintain ventilatory support
 MANAGEMENT OF
NEUROGENIC SHOCK
• Observe for Bradycardia-major
dysrhythmia
• Observe for DVT- venous pooling in extremities
make patients high-risk>>P.E.
• Use prevention modalities [TEDS, ROM,Sequential
stockings, anticoagulation]
NURSING DIAGNOSIS
• Fluid Volume Deficit r/t relative loss
• Decreased CO r/t sympathetic blockade
• Anxiety r/t biologic, psychologic or social integrity
Management Neurogenic Shock

– Alpha agonist to augment tone if perfusion

still inadequate
• dopamine at alpha doses (> 10 mcg/kg per min)
• ephedrine (12.5-25 mg IV every 3-4 hour)
– Treat bradycardia with atropine 0.5-1 mg
doses to maximum 3 mg
• may need transcutaneous or transvenous pacing
temporarily
 SEPSIS
• Systemic Inflammatory Response (SIRS) to
INFECTION manifested by two or > of following:
– Temp > 38 or < 36 centigrade
– HR > 90
– RR > 20 or PaCO2 < 32
– WBC > 12,000/cu mm or > 10% Bands (immature wbc)
 SEPTIC SHOCK
• SEPSIS WITH:
• Hypotension (SBP < 90 or > 40 reduction from
baseline) &
• Tissue perfusion abnormalities invasion of the
body by microorganisms & failure of body’s
defense mechanism.
Risk Factors Associated with Septic
Shock
• Age • Use of invasive
catheters
• Malnutrition
• Traumatic wounds
• General debilitation
• Drug Therapy
 Pathophysiology of Septic shock
• Initiated by gram-negative (most common) or gram
positive bacteria, fungi, or viruses
è Cell walls of organisms contain Endotoxins
è Endotoxins release inflammatory mediators
(systemic inflammatory response) causes…...
è Vasodilation & increase capillary permeability leads
to
è Shock due to alteration in peripheral circulation &
massive dilation
 Pathophysiology of Septic Shock
IMMUNE / INFLAMMATORY RESPONSE
Microorganisms enter body


Mediator Release

Activation of Complement, kallikrein / kinin/ coagulation
& fibrinolytic factors platelets, neutrophils & macrophages>>damage to endothelial
cells.
ORGAN DYSFUNCTION
 Clinical Presentation Septic Shock

• Two phases:
– “Warm” shock - early phase
• hyperdynamic response, VASODILATION
– “Cold” shock - late phase
• hypodynamic response
• DECOMPENSATED STATE
 Clinical Manifestations
• EARLY---HYPERDYNAMIC
STATE---COMPENSATION

– Massive vasodilation – Decreased SVR*

– Pink, warm, flushed – Increased CO & CI
skin – SVO2 will be
– Increased Heart Rate abnormally high
Full bounding pulse – Crackles
– Tachypnea
 Clinical Manifestations
• L ATE--HYPODYNAMIC
STATE--DECOMPENSATION
– Vasoconstriction – Increase SVR
– Skin is pale & cool – Decreased CO
– Significant tachycardia – Decreased UOP
– Decreased BP – Metabolic &
respiratory acidosis
with hypoxemia
 COLLABORATIVE MANAGEMENT

• Prevention !!!
• Find and kill the source • Maximize O2 delivery
of the infection Support
• Fluid Resuscitation • Nutritional Support
• Vasoconstrictors • Comfort & Emotional
• Inotropic drugs support
 Sequelae of Septic Shock

• The effects of the bacteria’s endotoxins can

continue even after the bacteria is dead!!!
 Cairan nutrisi – Nutrisi Parenteral
• Protein 4kcal/g
Nutrien Utama • Karbohidrat 4kcal/g (enteral)
3,4kcal/g (parenteral)
• Lemak 9kcal/g

Tambahan Vitamin
• Larut dalam air
• Larut dalam lemak
Mineral
• Elektrolit
• Trace elements dan ultra trace
minerals
 • Berdasarkan : Massa tubuh, Umur dan tipe protein
• Kebutuhan harian :
 Sehat 0.8-1.0 g/kg/hari
Protein  Stress 1.0-2.0 g/kg/hari (tergantung kondisi)

• Sumber atas 50%-60% kalori total

• Mempertahankan anabolisme protein
Karbohidrat • Menghasilkan 4kcal/g (enteral), 3,4kcal/g (parenteral)

• Sumber energi dan asam lemak esensial

 Linoleic acid : 2-7 g/hari
• Sumber atas 20%-30% kalori total
Lemak

Kalori
Total
Perubahan Distribusi Kalori pada Proses Katabolisme
Pemberian nutrisi baik secara total
maupun parsial secara intravena
 Karbohidrat

Formulasi karbohidrat parenteral :

• Mengandung 3.4kcal/g
• Dapat menjadi sumber kalori (energi) tunggal
• Kecepatan pemberian tidak dapat melebihi 5mg/kg/menit
• Berhubungan erat dengan osmolalitas larutan

Contoh sediaan karbohidrat parenteral:

• Triofusin 500/1000/1600 ®
• Tutofusin OPS ®
• Triparen 1/2®
 Asam Amino
Formulasi asam amino parenteral :
• Konsentrasi bervariasi antara 2,5%-15%
• Kandungan energi 4 kcal/g
• Nitrogen (g) = protein (g)/6.25

Beberapa sediaan asam amino parenteral di Indonesia :

• Asam amino 2,5% : Pan Amin G®.
• Asam amino 5% : Aminofusin L®, Aminoplasmanal 5% E®, Aminosteril 5%®,
Aminovel 600® , Nutrisol-S 5%®.
• Asam amino 10% : Aminoplasmanal 10%®, Amiparen®, Primene 10%®.