SYOK

SHOCK
SYOK : Sirkulasi inadekwat Gagal perfusi

jaringan Dapat menyebabkan gagal organ

Aliran darah keorgan yg tidak adekwat
Hipotensi diikuti hipoperfusi
Ketidak seimbangan V02 & D02

.
Shock can be result of

-poor oxygen delivery

-maldistribution of blood flow
-the effect of cytokines on cell function
-a low perfusion pressure
-or a combination of these factors
The common denominator in all shock
states and the earliest manifestation of
shock is reduced oxygen consumption
(VO2)

FUNGSI MITOCHONDRIA
1. Pembentukan ATP
2.Pengaturan ion Ca++ intraseluler
3.Sensor oksigen
4.Inisiatif awal program apoptosis dan nekrosis sel
5.Steroidogenesis dan sinyaling

.
Cellular hypoxia can incite

Systemic Inflammatory Respon

Syndrome

Two or more conditions

*Temperature > 38o C or < 36o C

*HR > 90x/min.

*RR > 20 or PaCO2 < 32 torr

*WBC > 12.000, <4.000 or<10%

immature forms
Multiple Organ Dysfunction
Syndrome

The oxygen debt is caused by

*A low flow : in hypovolemic and

cardiogenic shock
*A cellular or metabolic deficit :
in septic shock
*A maldistribution of blood flow :
in other types of shock

Shock states
Released various cytokines and interplay

with various organ systems to cause end

organ damage or MODS.
Cytokines : NO-nitric oxide

IL-2

TNF
respiratory failure, capillary leak,
shunting, redistribution, depressed
myocardial function, oxygen uncoupling, and
cellular ischaemia

The mediator response in SIRS

1. Induction
2. Triggering of cytokines synthesis
3. Evolution of cytokines cascade
4. Elaboration of secondary

mediators with ensuing cellular

injury
Example :

Endotoxin phagocytic cells (macrophag)

TNF- activate complement coagulation

cascades & induces endothelial cell activation

Hemodynamic profiles of shock

Type of shock

PAOP
C.O
SVR
----------------------------------------------------------Cardiogenic

Hypovolemic

Distributive
or N
or N or
Obstructive
or N or

PAOP pulmonary artery occlusion pressure

CO
cardiac output
SVR

systemic vascular resistance

EVALUATION OF SYMPTOMS

HISTORY

In cardiogenic shock : cardiac disease, poor

cardiac function,CHF, myocardial isch.,

valvular heart disease.
In hypovolemic shock : blood loss, trauma,
fluid losses, dehydration, third spacing or
other fluid losses.

History
In distributive shock : infection or allergic

agent, neurologic events or a reaction to

various immunologic substance.
In obstructive shock : trauma cardiac
tamponade, tension pneumothorax
In adult drop Systolic BP > 40 mmHg

significant hypotension

General Symptoms of Shock

CNS changes

*Confusion, coma, combative behavior,

agitation, stupor
Skin changes

*Cool, clammy, warm, diaphoresis

Cardiovascular

*Increase or decrease heart rate,

arrhythmia, angina, low high or normal

cardiac output, changes in pulmonary

pressure

General symptoms of shock

Pulmonary
*Increased RR, increase or decrease in
end- tidal CO2, decrease O2 saturation,
increased pulmonary pressures,
respiratory failure, decreased tidal

volume,
decreased FRC
RENAL
*Decreased urine output, elevation in BUN
and creatinine levels, change in urine
electrolyte levels

Common effects of shock on organs

Systemic : Capillary leak, formation of

micro
vascular shunts, cytokine release
Cardiovascular : circulatory failure,

depression of cardiovascular function

, arrhythmia
Haematologic : bone marrow suppression,

coagulopathy, DIC, platelet

dysfunction

Hepatic : liver insufficiency, elevation of

liver enzyme levels, coagulopathy

Neuroendocrine : change in mental status,

adrenal suppression, insulin

resistance, thyroid dysfunction

Renal : renal insufficiency, change in urine

electrolyte levels, elevation of BUN

and creatinine levels

Cellular : cell-to-cell dehiscence, cellular

swelling, mitochondrial dysfunction,

cellular leak

Hypovolemic shock
Cause : depletion of fluid in the intravascular

space (hemorrhage, vomiting, diarrhea,

dehydration, capillary leak or a
combination)
SIRS capillary leak
Findings : decreased CO, decreased PCWP,
increase SVR
Echo : decreased right-sided filling,
decreased stroke volume, increase aortic
diameter

Perdarahan
Kehilangan akut darah dari sistim sirkulasi
Volume darah normal :
* Dewasa : 7% BB ideal
*Anak : 8-9% BB ideal

Perdarahan
Mulai segera resusitasi cairan agressif
Pengobatan disesuaikan dengan respon

pasien pada terapi awal

Tanda perdarahan

Klas I

-----------------------------------------------------------

Perdarahan ml
Perdarahan (%BV)
Nadi
Tensi
Tek Nadi (mmHg)
Nafas
Urine ml/jam
SSP/status mental
Penggantian cairan
(hukum 3:1)

sampai 750
sampai 15%
< 100
Normal
Normal atau naik
14 - 20
> 30
sedikit Cemas
Kristaloid

Tanda perdarahan

Klas II

-----------------------------------------------------------

Perdarahan ml
Perdarahan (%BV)
Nadi
Tensi
Tek Nadi (mmHg)
Nafas
Urine ml/jam
SSP/status mental
Penggantian cairan
(hukum 3:1)

750-1500
15-30%
>100
Normal
Turun
20-30
20-30
Cemas sedang
Kristaloid

Tanda perdarahan

Klas III

-----------------------------------------------------------

Perdarahan ml
Perdarahan (%BV)
Nadi
Tensi
Tek Nadi (mmHg)
Nafas
Urine ml/jam
SSP/status mental
Penggantian cairan

darah
(hukum 3:1)

1500-2000
30-40%
> 120
Turun
Turun
30-40
5-15
Cemas gelisah
Kristaloid &

Tanda perdarahan
Klas IV

-----------------------------------------------------------

Perdarahan ml
Perdarahan (%BV)
Nadi
Tensi
Tek Nadi (mmHg)
Nafas
Urine ml/jam
SSP/status mental
Penggantian cairan

darah

(hukum 3:1)

>2000
>40%
>140
turun
turun
>35
tak ada
gelisah/letargi
kristaloid &

Perdarahan bermakna
perlu konsultasi BEDAH
.

Keputusan Pengobatan
Respon pasien pada resusitasi cairan merupakan

penentu terapi berikutnya

INGAT
Bedakan antara hemodinamik stabil dan
hemodinamik normal

Keputusan Terapi
Respon cepat
*< 20% perdarahan
*Stabil : respon pada penggantian cairan
*Lanjutkan monitor
*Evaluasi dan konsultasi bedah

Keputusan Terapi
20-40% perdarahan
Tidak stabil : memburuk setelah terapi cairan awal
Lanjutkan cairan dan darah
Evaluasi dan konsultasi bedah
Perdarahan berlanjut : operasi

Keputusan terapi
Tak ada respon (minimal)
> 40% perdarahan
Tak ada respon pada terapi cairan
Singkirkan kemungkinan shock nonhemorrhagik
Operasi segera

Diagnosis & pengobatan

Pitfalls
*Tensi tidak sama dengan cardiac output
*Umur
*Atlit
*Hipotermi
*Pengobatan
*Pacu-jantung

Distributive shock
Septic shock
Anaphylactic shock, acute adrenal insufficiency,

neurogenic shock.
Problem : shunts and capillary leak
Haemodynamic : normal/increased CO, low SVR
Low-to-normal LVFP
Echo : low SV, increase aortic diameter

Mitochondria pada sepsis

Terjadi gangguan morphologi (integritas membrane)

mitochondria jantung setelah 24 jam sepsis Gram

negative
(Circ shock 1992,26:452-560)
Pembengkakan mitochondria otot rangka, setelah 18-48
shock endotoxin
(Virchows arch 1994; 424:653-659)
Fragmentasi dari membrane sel setelah 12-24 jam infeksi
Escherichia Coli

(shock 1996; 5:378-384)

 Terganggu fungsi respirasi dari mitochondria hepar

setelah 4 jam pemberian endotoxin

(Crit Care Med 2004; 32:478-488)
Isi mitochondria diaphragma berkurang sampai 50%
(Am J Phys Endocrinol Metab 2006; 291 E.

1044-50)

Mekanisme Gangguan Pada

Mitochondria

Mitochondria pada Sepsis

Obstructive shock
Direct mechanical obstruction to cardiac filling
Case : cardiac tamponade, massive increase in

intrathoracic pressure

Diagnostic testing
General laboratory : blood lactate, bicarbonate,

glucose, electrolyte Zn,Mg,Ca, BUN,

creatinine, liver enzymes, ABG analysis

Coagulation
Hematologic parameters
Renal parameters
Echocardiography

Complications of shock
Low flow tissue perfusion activating factor of SIRS

cytokines and vasoactives organ failure and

MODS.
Sensitive organ : Lung (ARDS), kidney (ARF)
If low flow state is not rapidly corrected other
organ dysfunction
Marker : metabolic acidosis or lactic acidosis
prolonged increased morbidity and mortality

Differential Diagnosis
Distributive shock
Hypovolemic shock
Obstructive shock
Cardiogenic shock

DD

Distributive shock :
Sepsis
Anaphylaxis
Anaphylactoid reactions
Neurogenic shock
Adrenal gland dysfunction
Trauma, burns and pancreatitis

DD
Hypovolemic shock
Dehydration (low fluid intake, diarrhea, bowel

obstruction, sweating or diabetes insipidus)

Diuresis (diuretics, hyperglycemia)
Capillary leak and third spacing (burns, sepsis,
pancreatitis, surgical stress)
Hemorrhage (trauma , GIT bleeding, fractures,
vascular injuries, ectopic pregnancy, etc)
Anemia

DD

Obstructive shock
Cardiac tamponade and restrictive pericarditis
Pulmonary embolism
Intrathoracic processes (pneumothorax, pulmonary

hypertension, diaphragmatic rupture)

DD
Cardiogenic shock
AMI
Septal infarctions
Cardiomyopathies (viral, alcoholic, infectious)

Management and Therapy

The basic goal of shock therapy is the restoration of

effective perfusion to vital organs and tissue before

the onset of cellular injury.
Basic resuscitation :
1.Rapid placement of a large- bore i.v line or a highflow central line as a route for fluid resuscitation
2. Secure the airway and high-flow oxygenation
oxygen saturation > 92%. Put on mechanical
ventilation if necessary
3.Foley catheter

General goals for support of shock patients

Hemodynamic support
MAP > 60-65 mmHg
PCWP= 15-18 mmHg
Cardiac index > 2.1 L/min per m2 of body surface

area for cardiogenic and obstructive shock

Cardiac index > 4.0 L/min per m2 body surface area
for septic, traumatic, or hemorrhagic shock

General goals
Optimization of oxygen delivery
Hb level > 10 g/dl
Arterial oxygen saturation > 92%
Reversal of organ system dysfunction
Maintain urine output > 0.5 ml/kg per hour

Therapy
Fluid management

Crystalloid, koloid and blood component

Vasoactive drugs
Monoclonal antibodies

Shock in children
CO = SV x HR
In children : the cardiac output is primarily

maintained by changes in heart rate.

Hypovolemia or decreased SVR compensate
with dramatic increase in the heart rate.
HR 160-200 x/min impending circulatory
failure
CO falls by 25% rapid decompensation
Bradycardia & hypotension uncompensated
shock rapidly irreversible shock.

Signs of Shock
Early

Late
----------------------------------------------------- Narrowed pulse pressure

Decreased systolic pressure

Orthostatic changes
Decreased diastolic pressure
(older patients)
Cold, pale skin
Delayed capillary filling
Altered mental status
Tachycardia
Confusion and lethargy
Hyperventilation
Diaphoresis

Decreased urine output

Classification and Etiologies of Shock

TYPE OF SHOCK

Hypovolemic:

Pump is empty

ETIOLOGY
Trauma (hemorrhage)

Dehydration (Vomiting

etc)
Metabolic disease (DM)

Excessive sweating (infant)

Cardiogenic: Weak/sick
Rhytm disturbances

pump
Congestive heart failure

Cardiomyopathy

Post-resuscitation

Classification and Etiologies of Shock

TYPE OF SHOCK

ETIOLOGY
------------------------------------------------------------ Distributive:
Sepsis

Anaphylaxis

Spinal cord injury

Third spacing of fluids

Obstructive: Obstruction
Tension pneumothorax

of outflow
Cardiac tamponade

Pulmonary embolism

Fluid distribution

Therapy of shock in children

Position
Oxygen
Intravenous access
Fluid
Reassess
Inotropes- Epinephrine, Dobutamine,

Dopamine
Cardiogenic shock
SVT: Adenosine or synchronized
cardioversion
VF: defibrillation

Note
The most common error in treating

shock is underestimating the severity of

the condition.
If there are signs of compensated
shock, treat early and aggressively to
prevent a bad outcome.
All patients require an IV, oxygen
therapy, and cardiopulmonary
monitoring.

Summary
Resuscitation of shock is based on

close monitoring and

hemodynamic support and
replacement of intravascular
volume.

Kelainan Elektrolit
Harus dilihat secara menyeluruh adanya kelainan

yang lain

Osmolarity = 2Na + glucose + BUN + ETOH

18
2.8
4.6

mosmol/Liter

Hyponatremia < 135 meq/L

Manifestasi klinik bila Na < 120

abdominal pain, headache, agitations,

hallucinations, cramps, confusion,
lethargy, seizures

Kausa hiponatremia
Hypotonic

Hypovolemic -- Extra renal

Renal losses
Euvolemic
Hypervolemic
Isotonic (pseudo)
Hypertonic

Hipernatremia Na > 150

Gejala bila osmolarity > 350

Irritability, ataxia
Lethargy, coma, seizure

Kausa hipernatremia
Loss of water

Reduced water intake

Water loss in excess of sodium

Gain of sodium

Hipokalemia K < 3.5

Bila K < 2.5

CNS -weakness, cramps, hiporefleksia

GIT ileus
CVS disritmia, worsening of digoxin toxicity
hipotensi/hipertensi
U waves, ST depression, prolonged QT
Renal metabolic alkalosis worsening hepatic
encephalopathy
Glucose intolerance

Kausa hipokalemia
Shift into the cell
Reduced intake
Increased loss

Renal loss
Miscellaneous
GI loss (vomiting, diarrhea, fistulas)

Hiperkalemia K > 5.5

Cardiac arrest
ECG : peak T wave, prolonged PR interval
VF, block
Neromuscular: weakness, paralysis
GIT : vomiting, colic, diarrhea

Kausa hiperkalaemia
Factitious
Metabolic acidemia (acute)
Increased intake into the plasma
Oliguric RF
Impaired renin-aldosterone axis
Primary renal tubular potassium secretory defect
Inhibition of renal tubular secretion of K
Abnormal K distribution