Syock

Dr. Hariyono
2020
Shock is a complex syndrome that results when
tissue oxygenation or nutrient delivery are
insufficient to maintain the metabolic needs of the
Cell (Lorene, 2007)

Most commonly, this state is due to inadequate

tissue perfution but also result when the cell are
unnable to use available oxygen
Jika sel tidak menerima oksigen yang
cukup atau tidak bisa menggunakan
oksigen dengan baik maka terjadilah
metabolisme anaerob

Syok pada awalnya terjadi pada

tingkat sellular(mikro-sirkulasi) ,
kemudian berkembang ke tingkat
jaringan ,tingkat organ / multiple
(MOD) dan pada akhirnya
menyebabkan kematian
A. Glycolisis, metabolisme
anaerob
(tanpa oksigen),menghasilkan
asam piruvat--- asam laktat
dengan sedikit energy (2ATP) +
panas (32 Kcal)
B. Metabolisme aerobik lewat
siklus Crebb / asam cytric
asam piruvat dipecah
menjadi H2O dan CO2 +
energi tinggi (36 ATP) + panas
(417 Kcal)
Metabolisme Anaerobik,
Metabolisme apa yang
Anaerobik, apaterjadi ?
yang terjadi ?

Oksigenasi sel
Tidak adekwat

Inadequate
Anaerobic Lactic Acid
Energy
Metabolism Production
Production

Metabolic Metabolic
Cell Death!
Failure Acidosis
Penyebab:
Keadaan apapun yang membuat/mempengaruhi
kemampuan sistim sirkulasi untuk menyalurkan oksigen
( mikrosirkulasi )
Komponen pada sisitim sirkulasi :
1. Jantung --- sebagai pompa.
2. Darah + plasma----- sebagai pembawa oksigen ( +
nutrisi )
3. Pembuluh darah ---- sebagai wadah.
“ jika terjadi suatu masalah pada ke 3 komponen tersebut,
maka akan menyebabkan perfusi jaringan terganggu /
tidak adekwat “
Jantung
Sebagai pompa , memompa darah dari sistim vena ke paru
untuk oksigenisasi, dan memompakan darah yang
teroksigenisasi lewat arteri ke jaringan periperal.
Stroke Volume / isi volume sekuncup dipengaruhi :
1. Preload = jumlah darah yang diterima jantung
selama diastole
2. Contractility = kekuatan kontraksi otot jantung
“Hukum Frank starling”
3. Afterload = tahananan terhadap kontraksi
ventrikel.
- Contractility : dipengaruhi oleh hormon epineprin dan
norepineprin.
- Cardiac Out-put (CO) : jumlah darah yang dipompa
kan jantung selama 1 menit.
Cardiac Output = Stroke Volume X denyut 1 menit.
(HR)
- Tekanan darah : tahanan dari pembuluh peripheral
yang harus dilawan jantung ketika memompa darah.
tekanan darah = Cardiac Output X PVR/SVR
 Darah
Darah : berisi sel darah (ery,leu, platelets )
plasma, oksigen transports,
CO,nutrisi,hormon, zat sisa dan
panas harus dalam keadaan cukup.
- berkurangnya volume : pendarahan, dehidrasi
dsb. Menyebabkan syok
RESPON TUBUH TERHADAP SYOK / KOMPENSASI

• Normal compensation includes:

– Progressive vasoconstriction
– Increased blood flow to major organs
– Increased cardiac output
– Increased respiratory rate and volume
– Decreased urine output
Renin-Angiotensin-Aldosterone

Plasma
Kidney
volume
Detected by (juxtaglomerular
&/Or apparatus)

 [Na+] Releases
Via ACE
(Angiotensin
Converting Renin
Enzyme)
Converts

Angiotensin II…

Angiotensin I… Angiotensinogen
 Renin-Angiotensin-Aldosterone

 vasoconstriction  PVR
Angiotensin II…

 thirst

ADH
(anti-diuretic Fluid
 BP!
hormone) volume

Releases Na+
Adrenal
cortex Aldosterone reabsorption
 Cellular Response to Shock
O2 Tissue Impaired cellular
use perfusion metabolism

Anaerobic Stimulation of Impaired

metabolism clotting cascade & glucose
inflammatory usage
response
ATP
synthesis
 Intracellular Na+
& water Cellular edema
Na+ Pump
Function  Vascular volume
TAHAP-TAHAP SYOK

SYOK TERKOMPENSASI
SYOK TIDAK TERKOMPENSASI
SYOK YANG IRREVERSIBLE
 Compensated Shock

• Defense mechanisms are successful in

maintaining perfusion
• Presentation
– Tachycardia
– Decreased skin perfusion
– Altered mental status
 Uncompenstated Shock

• Defense mechanisms begin to fail

• Presentation
– Hypotension
– Prolonged Cap refill
– Marked increase in heart rate
– Rapid, thready pulse
– Agitation, restlessness, confusion
 Irreversible Shock

• Complete failure of compensatory

mechanisms
• Death even in presence of resuscitation
1. Shock Classification
Shock most often is categorized into four
basic types:
1. Hypovolemis
2. Cardiogenic
3. Distributive
4. Obstructive
The goal of therapy for all shock types is the
restoration of adequate tissue oxygenation while
preventing celluler necrosis and aorgan system
failure
Hypovolemic
Hypovolemic is the most common cause the
shock, this state is caused by a significant
reduction in whole blood or plasma volume
Traumatic bleeding, hemorrage from other causes,
severe burn, or general dehibration can produce
hypovolemic shock
Cardiogenik Shock
Cardiogenic shock result from a loss of miocaedial
contractility, leading in adequate cardiac out put
The heart can fail to be an ineffective pump in
cases of miocardial infarction, cardiac contution,
tamponade, myocarditis, Papilarry muscle
rupture, severe dysrhythmias, valvular disease
or cardiomyopathy
Distributive Shock
Distributive Shock occurs when venous polling,
occlusion of the microvasculer or poor blood flow
distribution limit tissue oxygenation
Three types of distributive shock are septik,
anaphylactive, and neurogenic
Septic Shock
Septik shock si the common form of distributive
shock. This state is produced by an
overwhelming infection that causes celluler
destruction, microvaskular occlusion, and
systemic vasodilatation
The sub sequent inadequate tissue perfution , third
spacing, and altered celluler metabolism affect
multiple organ
Anaphylactic shock
Anaphylactic shock is an acute, severe allergic
reaction stimulated by a profound antybody
response to an antigen
This reaction causes histamin release, increased
cappilary permiability, vasodilatation, smooth
muskle contraction, angiedema, and bronco
constriction
Neurogenic shock
Result from a loss of sympathetic tone, This state
leads to severe hypotention and unoposed vagal
responses that can cause bradycardia
Neurogenic shock is associated with acute spinal
cord disruption from traumatic injuries above the
level of T6
Obstructive shock
Is a form of indirect pump failure, the heart it self is
fine, but an external force decreases cardiac
output and inhibits pump function
Obstructive shock is caused by anything that
compresses the heart ( cardiac tamponade,
tension pneumothorax, or massive hemothorax)
or obstructs blood outflow (massive pulmonary
embolus, pulmonary hypertention, or savere
aortic stenosis)
Types of shock
Hypovolemic shock
Result from a loss of whole blood, plasma, or fluids
and electrolites
The following are common causes of hypovolemic
shock
Traumatic hemorrhage long bone or pelvic
fracture, solid organ rupture, and open wounds
Non traumatic hemorrhage  gastrointestinal
bleeding, rupture aortic aneurysm, rupture ectopic
pregnancy,posterior epistaxis, obstretic
hemorrhge and DIC
Fluid shifts : peritonitis, massive crush injuries,
severe burn
Non blod fluid loss : severe diarhea or vomiting,
exessive diaphoresis
Urinary fluid loss : Diabetic ketoacidosis,
diabetes incipidus, diuretic abuse
Clinical presentation in hypovolemic shock is
related to the amount and rate of actual volume
loss and includes the following sign and simtoms
Thachicardia
Hypotension
Orthostatic blood pressure
Narrowing pulse pressure
Tachypnea
Altered mental status, restlessness, anxiety, and
lethargy caused by decreased cerebral perfusion
Decreased central venous pressure, and
pulmonary artery wedge pressure
Reduced stroke volume, COP, and tissue
perfusion
Drop in renal perfusion with decreased urinary
output
Delayed capillary refill
Management of the patient in hypovolemic shock :
Support the patients airway, breathing, and
circulation
Administer oxygen saturation with continouos
pulse oximetri
Control bleeding if possible ( dressing, direct
pressure, and rapid surgery )
Initiate intra venous isotonic crystaloid infusion
- Cannulate two or more veins with large IV
catheters ( 14 – 16)
- Isotonic cristaloid are administered 3 : 1 (
300 ml of crystalloid for every 100 ml of
blood loss )
- Lactate ringers solution, normal saline,
and plasmalyte are examples of isotonic
crystalloid
- Isotonic solutions increase intravascular
volume and help maintain electrolyte
balance
- Lactate ringers solution is the crystalloid
most commonly used for initial hydration
- Infusing warmed fluids help minimize
hypothermia and subsequent metabolic
acidosis
Replace hemorrhagic losses with blood product
if the patient remains symtomatic after 3 – 4Lof
crystalloid
The use of vasopressor agent in patient with
acute volume depletion is not appropiate
Monitor the patient for any sign of complication
associated with infusion of blood product and
crystalloid
Prepare the patient for diacnostic studies and
surgical interventions
Insert an indwelling urinary catheter and urine
output
Place the patient on cardiac monitor. Check for
dysrhytmias
Monitor hemodynamis status
Keep the patient warm using blanket s, warming
lights
Insert a gastric tube to reduce gastric distention
 can stimulation the vagus nerve, causing
bradycardia
The development of hypovolemic shock
Hemorrhage or other fluid loss decreased intravascular vol

COP decrease

tissue perfution decrease

Compensatory mechanism are activated

Ephineprine and Renin angiotensin
Norephineprine release aldosteronesystem stimulation

Increased HR systemic Intracellular fluid shift to the IV space

vascular resistance

Increased blood vol

Increased COP

Compensatory Mechanism Fail

 Decreased COP

Decreased blood flow

Decrease perfusion of vital sign

MOF
Cardiogenic shock
The pump failure caused by cardiogenic shock
result in the inability of the heart to forcibly eject
sufficient blood to meet the tissue oxygenation
needs the body
This form of shock may be caused by acute
conditions such us myocardial infarction,
penetrating trauma, myocardial rupture,
dysrhytmia, or pericardial tamponade
Cardiogenic shock also can result from progessive
condition such as miocarditis or a
cardiomyopathy
When myocardial damage occurs, portion of the
myiocardium become dysfunctional
It thr damage area is large ( > 40 % of the
ventricle ), cardiac output decreases significantly
When the cardiac output is reduced, blood
pressure drops, tissue perfussion is inadequate
and the shock quickly follow
Clinical manifestation
Chest pain, diaphoresis, nausea, vomiting, syncope
ECG chage indicative of myocardiac ischemia, injury, or
necrose
Cardiac dysrhytmia
Rapid respiration
Hypoxemia
Decreased myocardial contractility
S3 and S4 heart sound
Reduced COP
Decreased level of consiousness
Cont…
Minimal urine output
Metabolic acidosis
Sign of left ventriculer failure
- Pulmonary edema caused by incomplete
emptying of the left ventricle
- Diffuse crackles and wheeze
- Decreased peripheral pulses
- Hypotension
Sign of right ventricular failure
- Jugular venous distention
- peripheral edema
- Hepatomegaly
Management of the patient in cardiogenic shock :
Support the patients airway, breathing, and
circulation
Intubate as necessary
Correct preload problem
- decreased preload : increase central
venous pressure , pulmonary artery wedge
pressure and pulmonary artery diastolic
pressure by administering intravenous
fluids
- increase preload : decrease central
venous prssure, pulmonary artery wedge
pressure and pulmonary artery diastolic
pressure with vasodilatory agent diuretic
Correct after load problems :
- Decrease after load : increase blood
pressure and systemic vascular resistance with
vasopressors
- Increase after load : decrease blood
pressure and systemic vascular resistance with
vasodilatory agent
Support myocardial contractility and cardiac
output
- Inotropic medications such as dopamine
and dobutamine increase contractility and
improve systolic BP
- An intra aortic ballon pump is a
percutaneously placed diastolic assist device
design to increase COP
Administer nitroglycerin IV to diminish
myocardial pain, increase coronary perfusion,
reduce preload and after load, decrase left
ventricular filling pressure
Give morphin sulphate to reduce pain and
anxiety, minimaze pulmonary edema , and
decrease after load
Use sodium nitroprusside (IV drip) to decrease
afterload (use cautiously in patients with
hypotension)
Administer diuretic (furosemide) to reduce
preload, reverse pulmonary edema, and improve
cardiac output
Give a beta blocker to decrease the heart rate
and increase cardiac filling time
Assist with insertion of pulmonary artery catheter
and arterial line to guide fluid administration and
drug titration
Administer antidysrhythmic agents and initiate
cardiac pacing as indicatet
Obtain an echocardiogram to quantify left
ventricular wall defects and evaluate valvular
function
Prepare the patient for coronary interventions
such as PTCA or coronary artery bypass graft
surgery
Distributive shock
This types of shock is characterized by an
abnormal distribution of intravascular volume as
result of decrease symphatetic tone and
increased vascular permeability
The three categories of distributive shock are
septic shock, anaphylactic and neurogenic
Septic shock
Result from the inflamatory responses of the body
to an everwhelming systemic infection
Septic shock usually is caused by gram negative,
gram positve, fungi, and viruses also have cited
as causes
The source of infection varies widely and may be
an indwelling urinary catheter, severe burn,
pneumonia, or post partum complication
Cont…
Other risk factor for septic shock include
immunosuppression, open large wound, and
gastrointestinal aschemia
Once they enter the circulation, gram negative
bacteria discharge endotoxin, the toxins trigger
release of chemical mediator, causing
vasodilatation, increased capillary permeability
The resulting inadequate tissue perfussion, third
spacing of fluid into the intertitium
Sign and symtoms of septic shock fall into two
phases :
Hyperdinamic phase (early, warm shock)
- The patient is febrile
- Flused, and pethechiae
- COP is significantly elevated
- Systemic vascular resistance is low due
to vasodilatation
- Tachycardia and tachypnea
- Systolic blood pressure is near normal, but
distolic pressure is low
- Mental status changes include, anxiety
and malaise
Hypodynamic phase (late, cold shock)
- temperature is subnormal
- respiration are rapid
- COP is low
- Hypotention and tachycardia
- Systemicvacular resistance is increased
bacause of profoun vasoconstriction
- Inadequate tissue perfussion causes the
skin to be cool
- Renal hypoperfussion decreased urynary
output (< 30 ml/hr)
Cont…
- Serum lactate levels are elevated,
reflecting anaerobic metabolism and lactic
acodosis
- Mental status changes include lethargy
and coma
Management of the patient in septic shock :
Support the patient airway, breathing, and
circulation
Provide supplemental oxygen to maintain a
PaO2
Restore intravascular volume with intravenoualy
administered crystalloid
Identify and remove potential sources of
infection
Obtain blood and wound cultures before
initiating antibiotic therapy
Begin timely antibiotic administration
- A combination of an aminoglycoside and a
third generation cephalosporin usually is ordered
initially
- Therapy is modified as infectious organism
are identified
- Use aminoglicosides cautiously in the elderly
and in other patient with renal insuffiency
Consider administration of drotrecogin alfa
(Xigris), a new agent for the treatment of sepsis
Administer an antyphiretic agent to warm
hypothermic patient with a body temperature
above 38 C
Positive initropic medication (dobutamine) may
be given to increase cardiac contractility and
output
Anaphylactic shock
Antigen antibody hypersensitifity reactin
resulting from reexposure to an antigen
Symtoms of anaphilactic are acute, sudden,
and rapidly progressive
The emergency nurse should look for the
following :
Respiratory difficulty
- Stridor
- Airway obstruction
- Bronchospasm
- Wheezing
Hypoxia
Hypotension
Tachycardia
Urticaria
Angioedema
Pruritus
Warm, dry skin that later becomes cool and plate
Abdominal pain and diarrhea
Dysrhytmias and cardias irritability
Respiratory and cardiac arrest
Management of the patient in anaphilactic shock
Aggresively support the patient airway, breathing
and circulation
Provide high floe oxygen, airway obstruction can
develop rapidly, so early intubation is indicated
Establish IV acces and administer crystalloid to
treat hypotension
Give ephineprine intra venous. This promotes
vasocontriction, dilated the bronchioles and
inhibist release of mediators
Administer a nebulized bronchodilator for
bronchospasm
Give diphenhidramine a histamine 1 blockers
and famotidine, a histamine 2 blocker to
decrease circulating histamine levels
Steroids such as methilprednisolone are used to
limit the inflammatory response
Crycothyroitomy may be required for severe
airway compromise
Neurogenic shock
Caused by decrease symphatetic tone following
spinal cord injury,or vasomotor center deppression
from head trauma
This condition also can result from the use of
certain adrenergic blocking agent
Neurogenic shock is associated with dilatation of the
arteriols and venules
The combination of low blood pressure and loos of
sympathetictone contributes to two significant clinical :
bradycardia, and warm, dry, flused skin
Clinical manifestation :
Hypotension
Tachypnea
Full, reguler pulse
Paraplegis or quadriplegia
Pale, cool above the tevel of the lesion
Priapism
Loss of sensation, motor function or reflex
A decreased level consiousnes because of
hypotension or brain injury
Normal urine output (initially)
Management of the patient in neurogenic shock :
Support the patient airway, bresthing and
circulation
Place the patient a supine position, blood
pressure will drop if the head of the bed is
elevated
Institute spinal immobilitation
Cive crystalloide IV expand intravascular volume
Intravenously administered vasopressors may be
used to help constrict the vascular and increase
BP
Cont…
Give atrophine IV for symtomatic bradycardia
Warm or cool the patient as needed to maintain
to normothermic core temperature
Obstructive shock
Is a pump failure that occurs as a result of force
external to the heart or an increase resistance to
venticular filling  pericardial tamponade,
tension pneumothorax
Management focuses on relieving the source of
obstruction anf providing basic supportive care,
including the following :
Support the patient airway, breathing and
circulation
Administer high flow oxygen
Establish IV acces
Symtoms and specific intervention associated with
various of obstructive shock :
Pulmonary embolism
- Sign and symtoms
- Dyspneu
- Tachypneu
- Chest pain
- Anxiety
- Hypoxemia
 Intervention
- Administer antycoagulant to the patient
- Administer of a fibrinolytic agent
- Surgical embolectomy
Coarctation of the aorta
Sign and symtoms
- Hypertension of the upper extremity with
hypotension in the lower extremity
 Intervention
- Prepare the patient for an aotugram, cardiac
catheterization, and surgical intervention
- IV acces
- Oxygen
Aortic stenosis
Sign and symtoms
- Chest pain
- Dyspneu
- Cyanosis
- Hypoxemia
- Cough and mental status changes
Intervention
- Prepare the patient for cardia
catheterization and surgical intervention
- IV acces
- Oxygen
- Supportive treatment of symtoms
 Conclusion
Although shock has many causes, the common
denominator in all shock states is an inability to
meet the demand for oxygen in the body.
Treatment involves measuer to increase cardiac
output and tissue perfusion to improve oxygen
delivery