SHOCK

Azaria Amelia Adam

TBM Komodo FK Undana

 DEFINITION
Disorder of tissue perfusion as a result of imbalance
between oxygen supply to and oxygen demand of the
cells.
All types of shock result in tissue perfusion disorder, which
may develop acute circulatory failure or it is also called
shock syndrome

IT IS NOT LOW BLOOD PRESSURE !!!

IT IS HYPOPERFUSION…..
SINDROMA KLINIS SYOK DITANDAI
DENGAN :
KEADAAN UMUM LEMAH
KULIT DINGIN, PUCAT, BASAH
VENA PERIFER YANG KOLAPS.
PENINGKATAN DENYUT NADI.
PENURUNAN TEKANAN DARAH.
PENURUNAN KESADARAN.
PENURUNAN PRODUKSI URINE.
YANG DISEBABKAN OLEH ADANYA GANGGUAN
PERFUSI ( ALIRAN DARAH ) DAN GANGGUAN
PENYAMPAIAN OKSIGEN KE JARINGAN.
 TYPES OF SHOCK*
Type of Shock Clinical causes Primary mechanism

Exogenous blood,
Hypovolemic Volume loss plasma, fluid or
electrolyte loss

Myocardial infarction,
Cardiogenic Pump failure cardiac arrhythmias,
heart failure

Increased venous Septic shock, spinal

Distributive capacitance or shock, autonomic
arteriovenous shunting blockade, drug
overdose
Vena caval obstruction,
Extra-cardiac
Obstructive cardiac tamponade,
obstruction of blood
pulmonary embolism,
flow
aortic compression or
dissection

*MORE THAN ONE TYPE MAY BE PRESENT

 1. HYPOVOLEMIC SHOCK
DECREASE IN INTRAVASCULAR
BLOOD VOLUME

Hemorrhage
Vomiting
Diarrhea
Fluid sequestration
Intraluminal – bowel obstruction
Intraperitoneal – pancreatitis
Interstitial - burns

DECREASE IN CARDIAC OUTPUT

AND TISSUE PERFUSION
HYPOVOLEMIC SHOCK
1. DECREASE IN INTRAVASCULAR
BLOOD VOLUME

2. BLOOD DIVERTED FROM SKIN TO

MAINTAIN ORGAN PERFUSION
Pale and cool skin
Postural hypotension and tachycardia

3. BLOOD DIVERTED PREFERENTIALLY

TO HEART AND BRAIN

Thirst, oliguria
Tachycardia
Labile blood pressure
HYPOVOLEMIC SHOCK
4. DECREASED BLOOD FLOW TO
BRAIN AND HEART

Restless, agitated, confused

Hypotension
Tachycardia
Tachypnea

5. END-STAGE SHOCK

Bradycardia
Arrythmias
Death
2. CARDIOGENIC SHOCK
DECREASED CARDIAC FUNCTION
Decreased ventricular function
MI (Myocardial infarction)
Pericaridal tamponade
Tension pneumothorax

Infective cardiac contraction

Arrhythmias

CLINICAL FINDINGS

Hypotension
Tachycardia
Tachypnea
Oliguria
**distended neck veins**
 3. SEPTIC SHOCK
SEVERE INFECTION W RELEASE OF
MICROBIAL PRODUCTS
Release of vasoactive mediators

HYPERDYNAMIC STATE
Peripheral vasodilation
Increased cardiac output

Fever, tachycardia, tachypnea, warm skin

MAINTENANCE OF FAILURE TO MAINTAIN

INTRAVASCULAR VOLUME INTRAVASCULAR VOLUME
Hyperdynamic shock Hypodynamic shock

Cool skin, tachycardia, hypotension,

oliguria
4. NEUROGENIC SHOCK
REDUCED VASOMOTOR TONE FROM
LOSS OF SYMPTATHETIC
INNERVATION
Spinal cord trauma
Spinal anesthesia
Acute gastric dilatation

CLINICAL FINDINGS

Bradycardia
Mild hypotension
Flat neck veins
HEMODYNAMIC
 Lung

Pulmonal
vein
Left atrium

SVR =
Systemic

Blood Pressure
Vascular
Right
Left Resistance
Atrium
ventricle

Right
ventricle

organ
PATHOGENESIS OF SHOCK
 Cardiogenic Distributive
Shock Shock
Inotropes
Vasopressor ( NE,PE,ADR,Dop)
(Dob,Dop,Adr,Amr)

Release Pump = Pipe = Vascular Blood Pressure

tamponade,etc
Heart

Obstructive Cardiac Output x SVR

Shock
Volume =
Blood

Hypovolemic
Fluids
Shock
 Pathophysiology of body
response to shock

 Neoroendocrine response
 Hemodynamic response
 Metabolic response
 FEAR
Stimulation of limbic Neuroendocrine response
area of brain
Adrenal cortex
Increased: Cortisol release
hypothalamic,
adrenomedullary
adrenocortical activity

R atrium Renal JGA

low-pressure stretch Renin release
receptors
LOSS OF TONIC
INHIBITION OF Pituitary gland
HYPOVOLEMIA CENTRAL AND ACTH, ADH and GH release
SYMPATHETIC
Aorta/carotids NERVOUS SYSTEMS Adrenal gland (medulla)
High-pressure Epinephrine/norepinephrine
baroreceptors release

Angiotensin II
Decreased renal
perfusion
Adrenal cortex
Aldosterone release
 HEMODYNAMIC RESPONSE
Mechanism to improve cardiovascular balance

 Blood flow redistribution

 Increased “cardiac output”

 Improve intravascular volume

 HEMODYNAMIC RESPONSE
BLOOD FLOW REDISTRIBUTION

HYPOTENSION

NEUROENDOCRINE STIMULATION

BLOOD FLOW PROTECTED BLOOD FLOW DECREASED

Heart Skin
Brain Muscle
Adrenal/pituitary gland Splanchnic circulation
 Limited to 180 beats/min
before decreased CO due
to decreased diastolic
filling time

CARDIAC OUTPUT = HR X SV

Increased
contractility Increase EDV via:
Venoconstriction
Arteriolar constriction
Renal reabsorption
Sympathetic n. system
Catecholamine release
 Improve blood volume
 Transcapillary refill phase
1. Decreased capillary pressure caused by hypotension
2. Sympathetic increase in precapillary arteriolar constriction

Decrease capillary hydrostatic pressure promotes passage of

fluid from interstitium to intravascular space

 Plasma protein restitution phase

Increased plasma osmolarity due to mainly hepatic release of
glucose, pyruvate, amino acids, etc.

Increased interstitial osmolarity

Increased interstitial volume and pressure

Transcapillary movement of albumin into intravascular space

 HEMODYNAMIC RESPONSE
Venoconstriction
Sympathetic n. system (SNS)
Catecholamines (CA) Reduced venous
Angiotensin II (ATII) capacitance
ADH

Arteriolar constriction
SNS, CA, ATII, ADH
Increased
ventricular
Decreased capillary P filling P

Fluid shift from interstitium into

vascular compartment Restoration of
blood volume
Increased distal tubular
reabsorption SV
Aldosterone, ADH

Increased proximal tubular

reabsorption
SNS, CA, ATII CO
Increased myocardial Increased ventricular
contractility
SNS, CA ejection fraction
BP
Increased heart rate
SNS, CA

Increased SVR due to

SVR
arteriolar construction
SNS, CA, ATII, ADH
 METABOLIC RESPONSE

 Hyperglycemia
 Lipid mobilization
 Protein catabolism / Protein breakdown
Increased urea synthesis
Increased aromatic amino acids

 Decreased acute phase reactant synthesis

 Increased extracellular osmolality
 METABOLIC RESPONSE
Release of:
Catecholamines
Cortisol Glycogen
Glucagon
Growth hormone breakdown
Conversion
of a.a. to
glucose
HYPERGLYCEMIA

Impaired
peripheral
glucose uptake Breakdown of
skeletal muscle
into a.a.
METABOLIC RESPONSE
Decreased blood
volume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysis
Pyruvate converted to lactic acid

METABOLIC ACIDOSIS
METABOLIC RESPONSE
Release of:
Catecholamines
Cortisol
Glucagon

LIPOLYSIS

INCREASE IN PLASMA FREE

FATTY ACIDS
 EFFECT OF SHOCK AT CELLULAR
LEVEL
LOW-FLOW,
POOR PERFUSION

HYPOXIA
ACIDOSIS

ANAEROBIC
METABOLISM

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.
 EFFECT OF SHOCK AT CELLULAR
LEVEL
CELL MEMBRANE FAILURE:
• DIRECT
Endotoxin
Complement
• INDIRECT
Failure to maintain normal Na+, K+ or Ca2+ gradient
Decreased oxidative phosphorylation

OSMOTIC
GRADIENT

Na+ entry Water entry CELLULAR IMPAIRED

into cell into cell EDEMA INTRACELLULAR
METABOLISM
EFFECT OF SHOCK AT ORGAN LEVEL

 Kidney
Oliguric renal failure
High output renal failure

 Liver
Liver failure

 GI tract
Failure of intestinal barrier (sepsis, bleeding)

 Lung
Capillary leak associated with or caused by sepsis and
infection
 DIAGNOSIS OF SHOCK STATUS
BASED ON HEMODYNAMIC
PARAMETER
CVP or Cardiac
TYPE PCWP Output SVR

Hypovolemic Decreased Decreased Increased

Cardiogenic Increased Decreased Normal or

Increased

Septic Decreased or Increased Decreased

increased
Traumatic Decreased Decreased or Decreased or
increased increased
Neurogenic Decreased Decreased Decreased

Hypoadrenal Decreased or Decreased or Decreased or

increased increased increased
 SUMMARY
 Shock is an altered state of tissue
perfusion severe enough to induce
derangements in normal cellular function
 Neuroendocrine, hemodynamic and
metabolic changes work together to
restore perfusion
 Shock has many causes and often may be
diagnosed using simple clinical indicators
 Treatment of shock is primarily focused
on restoring tissue perfusion and oxygen
delivery while eliminating the cause
TREATMENT OF RESPIRATORY FAILURE
Hypovolemia (blood loss)

Decreased CO

Decreased oxygen delivery, increased

oxygen requirement

Metabolic acidosis, hypoxemia tachypnea

TREATMENT:
Primary resuscitation
Oxygen
Mechanical ventilation if needed
 TREATMENT CONCEPT OF SHOCK
ENHANCING PERFUSION / OXYGEN DELIVERY

DO2 = CO x CaO2

Cardiac Arterial O2
output content

Oxygen delivery/DO2 = HR X SV X Hb X S02 X 1.34 + Hb X paO2

Inotropes Transfuse
Fluids Partially
dependent on
FIO2 and
pulmonary
status
APA ITU RESUSITASI CAIRAN ?

 RESUSITASI CAIRAN ADALAH PEMBERIAN SEJUMLAH

CAIRAN DALAM JUMLAH BESAR DENGAN WAKTU YANG
SINGKAT.
CAIRAN TUBUH

TERDIRI 60 % ( Total Body Water ) TERBAGI ATAS :

INTRA CELLULAR VOLUME ( ICV ) / [ICF], DIDALAM SEL
40 % BB.
EKSTRA CELLULAR VOLUME ( ECV ) / [ECF], DILUAR SEL
20 % BB.

ECV / ECF TERBAGI ATAS :

DALAM PEMBULUH DARAH ( PLASMA VOLUME ) 20 %
SISANYA DALAM INTERSTITIAL VOLUME ( ISV ) / [ISF].
 ION UTAMA

ECV : Na = 135 – 145 mEq / L ,

K = 4 – 5 mEq / L.
ICV : Na = 14 mEq / L
K = 157 mEq / L

KESEIMBANGAN DIANTARA ICV – ECV – PV

TERGANTUNG TEKANAN HIDROSTATIK,
TEKANAN ONKOTIK DAN TEKANAN OSMOTIK
MENGIKUTI HUKUM STARLING.
TRANSPORT O2

TAHAPAN :
PERNAFASAN ALVEOLI DIFUSI MASUK DARAH.
DARAH JARINGAN.
SISTIM O2 – Hb DALAM ERITROSIT JARINGAN.

 GANGGUAN OKSIGENASI O2 DALAM DARAH

BERKURANG ( HIPOKSEMIA )
 O2 DALAM JARINGAN BERKURANG (HIPOKSIA).
 ADA 4 JENIS HIPOKSIA :

HIPOKSIA – HIPOKSIK = GANGGUAN VENTILASI –

DIFUSI.
HIPOKSIA – STAGNAN = GANGGUAN PERFUSI /
SIRKULASI
HIPOKSIA – ANEMIK = ANEMIA
HIPOKSIA – HISTOTOKSIK = GANGGUAN PENGGUNAAN
O2 DI DALAM SEL (KERACUNAN HCN, SEPSIS)

 SHOCK KARENA PERDARAHAN

HIPOKSIA STAGNAN & HIPOKSIA ANEMIA
APAKAH PENDERITA ITU SHOCK ?
A. PERFUSI MENURUN.
PERIFER : DINGIN, PUCAT, BASAH,
CRT > 2 DETIK
GINJAL : PRODUKSI URINE MENURUN
SAMPAI ANURIA.
PERNAFASAN : RR ↓ / ↑
OTAK : GANGGUAN KESADARAN,
DELIRIUM, AGITASI – KOMA.
GI. TRACT : BISING USUS ( - ).
B. PENGISIAN NADI
MELEMAH
PADA SHOCK BERAT, NADI RADIALIS
SUKAR DIRABA.
C. TEKANAN DARAH TURUN
TEKANAN SISTOL TURUN 40 mmHg  HIPOTENSI
TENSI SISTOLIK 120 MmHg BELUM TENTU
TIDAK SHOCK.
TENSI SITOLIK 90 MmHg BELUM TENTU SHOCK
MAP = MEAN ARTERIAL PRESSURE DIATAS
65 – 70 MmHg.
SISTOLIK + 2 DIASTOLIK
3
APA PENYEBAB LAIN DARI SHOCK ?

PERDARAHAN
HYPOVOLEMIA

BUKAN PERDARAHAN
 TENSION PNEUMOTHORAK.
 TAMPONADE JANTUNG
 KARDIOGENIK
 NEUROGENIK
 SEPSIS
APA RESPON PENDERITA AKIBAT
PERDARAHAN ?

ESTIMATED BLOOD VOLUME ( EBV ) YANG

BEREDAR DALAM SISTIM SIRKULASI
KIRA – KIRA 70 CC / Kg BB.

1. TAKIKARDI.
2. PENINGKATAN KONTRAKSI MIOKARD DAN
VASOKONSTIKSI ARTERIAL DAN VENA

HORMON KATEKOLAMIN YANG MENINGKAT.

VASOKONTRIKSI

MEMERAS DARAH DARI CADANGAN VENA MASUK

SIRKULASI EFEKTIF UNTUK MENYELAMATKAN OTAK DAN
JANTUNG.
TAHANAN PEMBULUH DARAH MENINGKAT, KERJA
JANTUNG TAMBAH BERAT.
ISCHEMIC INJURY PADA ORGAN USUS ( MUKOSA )

TRANSLOKASI KUMAN MENEMBUS MUKOSA USUS

KUMAN MASUK SIRKULASI SISTEMIK ( BAKTERIMIA 

SEPSIS ).
3. TRANSCAPILARY REFILL

CAIRAN ISV MASUK KE PEMBULUH DARAH

DI MULAI 1 – 2 JAM SETELAH PERDARAHAN

( INTERNAL HEMODILUSI ). 100 – 120 CC / JAM.

4. PENINGKATAN KADAR HORMON ERITROPOETIN DAN

PENINGKATAN SINTESA PROTEIN PLASMA DI HATI.
 DERAJAD SHOCK KARENA PERDARAHAN
KLS 1 2 3 4
RR 14 - 20 20 - 30 30 - 40 >40

KULIT DINGIN DINGIN - PUCAT DINGIN, SIANOTIK

PUCAT,
BASAH
NADI < 100 > 100 > 120 >140 -
TAK TERABA
TENSI NORMAL - SISTOLIK TETAP SISTOLIK SANGAT ↓ TAK
POSTURAL DIASTOLIK ↑ TURUN TERUKUR
HIPOTENSI TEK. NADI ↑

KESADARAN NORMAL GELISAH / GELISAH - TAK SADAR

DELIRIUM AGITASI LETHARGY
PRODUKSI NORMAL TURUN OLIGURI ANURIA
URINE
KEHILANGAN S/D 15 – 30 % EBV 30 – 40 % > 40 % EBV
DARAH 15 % EBV EBV
 Estimated Blood Volume

 Preterm neonate : 95ml/kgBB

 aterm neonate : 90ml/kgBB
 Infant : 80ml/kgBB
 adult : 75ml/kgBB
APA YANG HARUS SAYA LAKUKAN ?
 BERI OKSIGEN
 Posisi syok
 STOP PERDARAHAN
LUKA TERBUKA BEBAT TEKAN. (
DIRECT PRESSURE ) PADA TEMPAT LUKA, JANGAN
DI TORNIQUET, JANGAN DI KLEM.
LUKA TERTUTUP CEK 5 TEMPAT
THORAK
ABDOMEN
PELVIS
RETROPERITONEAL
TULANG PANJANG
BERI VOLUME ( CAIRAN REPLACEMENT )

TRANFUSI
PALING BAIK
PERLU CROSS – MATCH DAN SCREENING.
TIDAK SELALU BEBAS PENYAKIT
REAKSI TRANSFUSI.
 KRISTALOID

ADALAH CAIRAN YANG MENGANDUNG ELEKTROLIT (

RINGER LACTAT/RL ), NORMAL SALIN ( NaCl 0,9% ),
RINGER ACETAT.
DIBERIKAN SEJUMLAH 2 – 4 X DARI PERKIRAAN DARAH
YANG HILANG DARI PEMBULUH DARAH.
KRISTALOID MERESAP MASUK KE INTERSTITIEL CELL 30
– 60 MENIT SESUDAH INFUS.
 EKSPANSI INI OEDEMA  HILANG DLM 1 – 2 HARI.
 OEDEMA PADA PALPEBRA  EXCES 2 – 3 Lt.
 OEDEMA PADA PARU DAPAT TERJADI PADA PASIEN
DENGAN / TANPA KONTUSIO PULMONUM.
 PEMBERIAN CAIRAN BUKAN DARAH

EKSTERNAL HEMODILUSI ( HEMODILUSI )

HEMODILUSI DENGAN KRISTALOID DIBATASI BILA :

Hb KURANG DARI 7 Gr %.

ALBUMIN KURANG DARI 2 Gr %
ADA TRAUMA KEPALA ( COB ).
ADA TRAUMA THORAK ( CONTUSIO PARU ).
 KOLOID

CAIRAN DENGAN BM 35000 – 500.000

MEMILIKI EFEK MIRIP ALBUMIN  NILAI ONKOTIKNYA
TINGGI SEHINGGA TINGGAL LAMA DALAM PEMBULUH
DARAH.
TEKANAN DARAH DAPAT KEMBALI NORMAL LEBIH
CEPAT.
 TIDAK TEPAT DIBERIKAN SEBAGAI TERAPI AWAL
ATAUPUN TERAPI TUNGGAL PENGGANTI PERDARAHAN
 DAPAT MENYEBABKAN REAKSI ANAFILAKTIK.
 MAHAL.
 BOLEH DIBERIKAN SETELAH CAIRAN KRISTALOID

PASANG CATHETER URINE

APA YANG DIEVALUASI SETELAH DIBERI CAIRAN ?
1. KESADARAN MEMBAIK

2. PRODUKSI URINE > 1CC / Kg BB / JAM

3. KULIT HANGAT, KERING,

CAPILLARY REFILL TIME

4. RESPIRASI NORMAL 16 – 20 X

5. VITAL SIGN KEMBALI NORMAL

 APA PERANGKAP ( PIT FALLS )
DARI SHOCK ?
1. USIA TUA
2. ATLETIK
3. IBU HAMIL
4. PEMAKAI OBAT – OBATAN PENYEKAT BETA ( BETA
BLOCKERS ).
5. HIPOTERMIA
6. HEMOGLOBIN
 KESIMPULAN
 BERI OKSIGEN
 STOP PERDARAHAN
 BERIKAN CAIRAN ELEKTROLIT SAMPAI NORMOVOLEMIA
(END-POINT OF FLUID RESUSCITATION ) BUKAN SAMPAI
NORMOTENSI
 EVALUASI ULANG