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SYOK
SYOK

Virgianti NF, M.Kep, Ners

DEFINISI

  • suatu syndroma dimana perfusi

jaringan tidak adekwat, akibat dari ketidak mampuan sistim

sirkulasi untuk mensuplai oksigen

  • 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
  • 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, apa yang terjadi ? Oksigenasi sel Tidak adekwat
Metabolisme Anaerobik, apa yang terjadi
?
Oksigenasi sel
Tidak adekwat
Metabolisme Anaerobik, apa yang terjadi ? Oksigenasi sel Tidak adekwat Inadequate Energy Production Metabolic Failure Anaerobic

Inadequate

Energy

Production

Metabolic

Failure

Metabolisme Anaerobik, apa yang terjadi ? Oksigenasi sel Tidak adekwat Inadequate Energy Production Metabolic Failure Anaerobic
Anaerobic Metabolism
Anaerobic
Metabolism

Lactic Acid Production

Metabolisme Anaerobik, apa yang terjadi ? Oksigenasi sel Tidak adekwat Inadequate Energy Production Metabolic Failure Anaerobic
Metabolisme Anaerobik, apa yang terjadi ? Oksigenasi sel Tidak adekwat Inadequate Energy Production Metabolic Failure Anaerobic

Cell Death!

Metabolisme Anaerobik, apa yang terjadi ? Oksigenasi sel Tidak adekwat Inadequate Energy Production Metabolic Failure Anaerobic
Metabolic Acidosis
Metabolic
Acidosis
Penyebab:
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 “

Komponen sistim sikulasi

Komponen sistim sikulasi
Jantung  Sebagai pompa , memompa darah dari sistim vena ke paru untuk oksigenisasi, dan memompakan
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.
Hukum Frank-Starling “ peregangan serabut miokardium selama diastole melalui peningkatan volume akhir diastole akan meningkatkan kontraksi
Hukum Frank-Starling
“ peregangan serabut miokardium
selama diastole melalui peningkatan
volume akhir diastole akan
meningkatkan kontraksi pada saat
sistole “

- 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
Darah Darah : berisi sel darah (ery,leu, platelets ) plasma, oksigen transports, CO,nutrisi,hormon, zat sisa dan

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
-
berkurangnya volume : pendarahan,
dehidrasi dsb. Menyebabkan syok
Pembuluh darah.
Pembuluh darah.
 Dibawah pengaruh outonom.  Kebocoran = gangguan perfusi.
Dibawah pengaruh outonom.
Kebocoran = gangguan perfusi.

RESPON TUBUH TERHADAP SYOK / KOMPENSASI

Progressive vasoconstriction Increased blood flow to major organs Increased cardiac output Increased respiratory rate and volume Decreased urine output

Normal compensation includes:

Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Releases Renin Converts Detected by &/Or  [Na+] Via ACE
Renin-Angiotensin-Aldosterone
Renin-Angiotensin-Aldosterone
Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Releases Renin Converts Detected by &/Or  [Na+] Via ACE
Plasma volume
Plasma
volume
Kidney (juxtaglomerular apparatus) Releases
Kidney
(juxtaglomerular
apparatus)
Releases
Renin Converts
Renin
Converts

Detected by

Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Releases Renin Converts Detected by &/Or  [Na+] Via ACE
Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Releases Renin Converts Detected by &/Or  [Na+] Via ACE

&/Or

Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Releases Renin Converts Detected by &/Or  [Na+] Via ACE
 [Na+]
 [Na+]

Via ACE (Angiotensin Converting Enzyme)

Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Releases Renin Converts Detected by &/Or  [Na+] Via ACE
Angiotensin II…
Angiotensin II…
Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Releases Renin Converts Detected by &/Or  [Na+] Via ACE
Angiotensin I…
Angiotensin I…

Angiotensinogen

Renin-Angiotensin- Aldosterone  vasoconstriction  PVR Angiotensin II…  thirst
Renin-Angiotensin-
Aldosterone
 vasoconstriction
 PVR
Angiotensin II…
 thirst
Renin-Angiotensin- Aldosterone  vasoconstriction  PVR Angiotensin II…  thirst Adrenal cortex ADH (anti-diuretic hormone) Releases
Renin-Angiotensin- Aldosterone  vasoconstriction  PVR Angiotensin II…  thirst Adrenal cortex ADH (anti-diuretic hormone) Releases
Renin-Angiotensin- Aldosterone  vasoconstriction  PVR Angiotensin II…  thirst Adrenal cortex ADH (anti-diuretic hormone) Releases
Adrenal cortex
Adrenal
cortex
ADH (anti-diuretic hormone)
ADH
(anti-diuretic
hormone)

Releases

Renin-Angiotensin- Aldosterone  vasoconstriction  PVR Angiotensin II…  thirst Adrenal cortex ADH (anti-diuretic hormone) Releases
Fluid  BP! volume
Fluid
 BP!
volume
Na+ reabsorption
Na+
reabsorption
Aldosterone
Aldosterone
Renin-Angiotensin- Aldosterone  vasoconstriction  PVR Angiotensin II…  thirst Adrenal cortex ADH (anti-diuretic hormone) Releases
Renin-Angiotensin- Aldosterone  vasoconstriction  PVR Angiotensin II…  thirst Adrenal cortex ADH (anti-diuretic hormone) Releases
Cellular Response to Shock O 2 use Anaerobic metabolism ATP synthesis Na + Pump Function Tissue
Cellular Response to Shock
Cellular Response to Shock
O 2 use
O 2
use
Cellular Response to Shock O 2 use Anaerobic metabolism ATP synthesis Na + Pump Function Tissue
Anaerobic metabolism ATP synthesis Na + Pump Function
Anaerobic
metabolism
ATP
synthesis
Na + Pump
Function
Tissue Impaired cellular perfusion metabolism Stimulation of clotting cascade & inflammatory response Impaired glucose usage 
Tissue
Impaired cellular
perfusion
metabolism
Stimulation of
clotting cascade &
inflammatory
response
Impaired
glucose
usage
 Intracellular Na +
& water
Cellular edema
 Vascular volume
TAHAP-TAHAP SYOK
TAHAP-TAHAP SYOK
 SYOK TERKOMPENSASI  SYOK TIDAK TERKOMPENSASI  SYOK YANG IRREVERSIBLE
SYOK TERKOMPENSASI
SYOK TIDAK TERKOMPENSASI
SYOK YANG IRREVERSIBLE
Compensated Shock • Defense mechanisms are successful in maintaining perfusion • Presentation – Tachycardia – Decreased
Compensated Shock
Compensated Shock

Defense mechanisms are successful in maintaining perfusion Presentation

Tachycardia Decreased skin perfusion Altered mental status

Uncompenstated Shock – Hypotension – Prolonged Cap refill – Marked increase in heart rate – Rapid,
Uncompenstated Shock
Uncompenstated Shock

Hypotension Prolonged Cap refill Marked increase in heart rate Rapid, thready pulse Agitation, restlessness, confusion

Defense mechanisms begin to fail Presentation

Irreversible Shock • Complete failure of compensatory mechanisms • Death even in presence of resuscitation
Irreversible Shock
Irreversible Shock

Complete failure of compensatory mechanisms Death even in presence of resuscitation

SHOCK CLASSIFICATION (FCCS, 2001)

. HYPOVOLUMIC SHOCK: blood loss, git loss, third space loss

-CARDIOGENIC SHOCK -OBSTRUCTIVE SHOCK: cardiac tamponade, pulmonary embolism -DISTRIBUTIVE SHOCK: anaphylactic,neurogenic, acut adrenal insufficiency

Hypovolemic Shock

Penyebab : kehilangan cairan intravascular

Internal atau external hemorrhage. Trauma. Dehydration. Plasma loss from burns. Excessive sweating. Diabetic ketoacidosis with resultant osmotic diuresis.

Tanda dan gejala shok

-Penurunan kesadaran :

-Nadi : mula-mula meningkat, sampai tak teraba -Hypoperfusi : Capillary refill memanjang, acral dingin / basah. -Produksi urine menurun < 0.5 1ml/kg/jam. -Tekanan darah mula-mula normal, kemudian menurun. -Dysarithmia

MANAGEMEN SYOK HIPOVOLUMIK

-AIRWAY

-BREATHING

-CIRCULATION

AND

HEMORRHAGE

MANAGEMEN SYOK HIPOVOLUMIK - AIRWAY - BREATHING - CIRCULATION AND HEMORRHAGE CONTROL - SHOCK POSITION -
MANAGEMEN SYOK HIPOVOLUMIK - AIRWAY - BREATHING - CIRCULATION AND HEMORRHAGE CONTROL - SHOCK POSITION -

CONTROL

MANAGEMEN SYOK HIPOVOLUMIK - AIRWAY - BREATHING - CIRCULATION AND HEMORRHAGE CONTROL - SHOCK POSITION -

-SHOCK POSITION -REPLACE BLOOD LOSS -STOP / MINIMIZE THE BLEEDING PROCESS

AIRWAY

Open airway : head tilt & chin lift , modification jaw trust(trauma)

Secure airway: Oro-pharingeal , naso-pharyngeal . ETT

Control secret : Rigid suction cateter ( Yangkeur ) for Trauma Px

AIRWAY Open airway : head tilt & chin lift , modification jaw trust(trauma) Secure airway: Oro-pharingeal
AIRWAY Open airway : head tilt & chin lift , modification jaw trust(trauma) Secure airway: Oro-pharingeal

BREATHING

AIR pO2 150

20,9% O2 + 80% N2

BREATHING AIR pO2 150 20,9% O2 + 80% N2 ALVEOLI 16% 02 + 80% N2 +

ALVEOLI

16% 02 + 80% N2 + 4% CO2

pO2 120

BREATHING AIR pO2 150 20,9% O2 + 80% N2 ALVEOLI 16% 02 + 80% N2 +

DARAH pO2 100

Hypoxia = paO2 < 90mmhg

Terapi Oksigen = meningkatkan paO2 dengan cara meningkatkan pO2 Udara

Onloading Oxygen in Lungs oxyhemeglobin pH 7.45 Remember: pH 7.4 CO 2  [H + ]
Onloading Oxygen in
Lungs
oxyhemeglobin
pH 7.45
Remember:
pH 7.4
CO 2  [H + ]
• pH shifts curve to left
• ‘onloading’ in lungs
deoxyhemeglobin

Pressure

Offloading Oxygen in Tissues oxyhemeglobin pH 7.4 Remember: CO 2  [H + ] pH 7.35
Offloading Oxygen in
Tissues
oxyhemeglobin
pH 7.4
Remember:
CO 2  [H + ]
pH 7.35
deoxyhemeglobin
•pH shifts curve to right
• ‘offloading’ to tissues
Pressure

Shock Position

Shock Position Live both foods If necessary up both arm “auto - transfusion” 300-500 cc
Shock Position Live both foods If necessary up both arm “auto - transfusion” 300-500 cc

Live both

foods

If necessary up both arm

Shock Position Live both foods If necessary up both arm “auto - transfusion” 300-500 cc
Shock Position Live both foods If necessary up both arm “auto - transfusion” 300-500 cc

“auto-transfusion” 300-500 cc

HYPOVOLUMIC SHOCK

HYPOVOLUMIC SHOCK SHOCK POSITION 2 LARGE I.V CATHETER LINE ( 14,16G ) TAKEN BLOOD SAMPLE RINGER

SHOCK POSITION 2 LARGE I.V CATHETER LINE ( 14,16G )

TAKEN BLOOD SAMPLE

HYPOVOLUMIC SHOCK SHOCK POSITION 2 LARGE I.V CATHETER LINE ( 14,16G ) TAKEN BLOOD SAMPLE RINGER

RINGER LAKTAT 1000 CC

HYPOVOLUMIC SHOCK SHOCK POSITION 2 LARGE I.V CATHETER LINE ( 14,16G ) TAKEN BLOOD SAMPLE RINGER

PERFUSION WARM,DRY,RED PULSE < 100 BP-SIST >100

HYPOVOLUMIC SHOCK SHOCK POSITION 2 LARGE I.V CATHETER LINE ( 14,16G ) TAKEN BLOOD SAMPLE RINGER

SLOW

POOR PERFUSION,BP- SIST<100, PULSE<100

HYPOVOLUMIC SHOCK SHOCK POSITION 2 LARGE I.V CATHETER LINE ( 14,16G ) TAKEN BLOOD SAMPLE RINGER

ADD RL UNTIL

3-4 X

EBF

BLOOD IF READY

Hemodilution technic

Estimate Wieght : 60 kg Estimate Blood volume: 70 ml/kg x 60 = 4200 ml Estimate blood loss : ---- % EBV = …… ml

BP-sist 120 100 <90 <60-70 Pulse 80 100 >120 >140/weak perfus warm pale cold Cold&wet -15%EBV
BP-sist
120
100
<90
<60-70
Pulse
80
100
>120
>140/weak
perfus
warm
pale
cold
Cold&wet
-15%EBV
-30%EBV
Normo
-50%EBV
volume
EBL
0
600
1200
2000 ml

Infusion

1200-2000

2500-5000

4000-8000ml

End-point of fluid resuscitation

-perfusion back to normal -BP (sistole) about 90 100 mmhg -Urine production 0,5 1 ml/kgBW/hour

NOT normal BP

----

re-bleeding risk !

Cardiogenic shock
Cardiogenic shock
 The heart loses its ability to supply all body parts with blood.  Usually the
The heart loses its ability to supply
all body parts with blood.
Usually the result of left ventricular
failure secondary to acute
myocardial infarction or CHF.
Many patients will have normal
blood pressures.

Cardiogenic Shock

Cardiogenic Shock R.A.S.  CO Activation  Catecholamine Release Volume/ Preload Myocardial O 2 demand Impaired
R.A.S.  CO Activation  Catecholamine Release
R.A.S.
 CO
Activation
 Catecholamine
Release
Cardiogenic Shock R.A.S.  CO Activation  Catecholamine Release Volume/ Preload Myocardial O 2 demand Impaired
Volume/ Preload
Volume/
Preload
Myocardial O 2 demand
Myocardial
O 2 demand
Cardiogenic Shock R.A.S.  CO Activation  Catecholamine Release Volume/ Preload Myocardial O 2 demand Impaired
Cardiogenic Shock R.A.S.  CO Activation  Catecholamine Release Volume/ Preload Myocardial O 2 demand Impaired
Impaired myocardial function
Impaired
myocardial function
Cardiogenic Shock R.A.S.  CO Activation  Catecholamine Release Volume/ Preload Myocardial O 2 demand Impaired
 SVR
 SVR
 O 2 supply Peripheral & pulmonary edema
 O 2
supply
Peripheral
& pulmonary
edema

Dyspnea

Cardiogenic Shock R.A.S.  CO Activation  Catecholamine Release Volume/ Preload Myocardial O 2 demand Impaired
Tanda dan Gejala
Tanda dan Gejala
 Edema paru akut : – Difficulty breathing. – As fluid levels rise, wheezes, crackles, or
Edema paru akut :
– Difficulty breathing.
– As fluid levels rise, wheezes,
crackles, or rales may be heard.
– There may be a productive cough
with white or pink-tinged foamy
sputum.
Cyanosis, altered mentation, and
oliguria.

MANAGEMENT OF CARDIOGENIC

SHOCK

-AIRWAY

-BREATHING

-CIRCULATION

MANAGEMENT OF CARDIOGENIC SHOCK - AIRWAY - BREATHING - CIRCULATION AND CARDIAC IMPROVING & MONITORING POSITION

AND

MANAGEMENT OF CARDIOGENIC SHOCK - AIRWAY - BREATHING - CIRCULATION AND CARDIAC IMPROVING & MONITORING POSITION

CARDIAC IMPROVING & MONITORING

MANAGEMENT OF CARDIOGENIC SHOCK - AIRWAY - BREATHING - CIRCULATION AND CARDIAC IMPROVING & MONITORING POSITION

POSITION +

-HEAD&SHOULDER UP

-IV.LINE WITH MINIMAL FLUID + KEEP WARM

-VASOPRESSOR , INOTROPIC AND DIURETIC ----- MAYBE NEEDED

DISTRIBUTIVE SHOCK
DISTRIBUTIVE SHOCK
 NEUROGENIC SHOCK  ANAPHYLAKTIC SHOCK  SEPTIC SHOCK
NEUROGENIC SHOCK
ANAPHYLAKTIC SHOCK
SEPTIC SHOCK

Neurogenic Shock

Results from injury to brain or spinal cord causing an interruption of

nerve impulses to the arteries. The arteries dilate causing relative

hypovolemia.

Sympathetic impulses to the adrenal glands are lost, preventing the release of catecholamines with their compensatory effects.

Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion
Neurogenic Shock
Neurogenic Shock
 Sympathetic Tone Or  Parasympathetic Tone
 Sympathetic Tone
Or
 Parasympathetic Tone

Vascular Tone

Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion
Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion
Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion

Massive Vasodilation

Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion
Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion
Tissue perfusion
Tissue
perfusion
Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion

Cardiac Output

Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion
Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion

SVR & Preload

Neurogenic Shock  Sympathetic Tone Or  Parasympathetic Tone  Vascular Tone Massive Vasodilation Tissue perfusion

TANDA &GEJALA

Warm, dry, red skin.

Tekanan Darah rendah

Bradycardia

Penatalaksanaan

Airway control.

Maintain body temperature.

Immobilization of patient.

Consider other possible causes

of shock.

IV access and medications that

increase peripheral vascular

resistance.

Anaphylactic Shock

A severe immune response to a

foreign substance.

Signs and symptoms most often occur within a minute, but can take up to an hour.

The most rapid reactions are in response to injected substances:

Penicillin injections.

Bees, wasps, hornets.

Anaphylactic Shock  “Container failure”  Massive & systemic allergic reaction  Large release of histamine
Anaphylactic Shock
Anaphylactic Shock
 “Container failure”  Massive & systemic allergic reaction  Large release of histamine  Increases
“Container failure”
Massive & systemic allergic reaction
Large release of histamine
Increases membrane permeability &
vasodilation

Tanda & Gejala

Because immune responses can affect different

body systems, signs and symptoms vary widely:

Skin:

Flushing, itching, hives, swelling, cyanosis.

Respiratory system:

Breathing difficulty, sneezing, coughing, wheezing, stridor, laryngeal edema, laryngospasm.

Tanda &Gejala

Cardiovascular system:

Vasodilation, increased heart rate, decreased blood pressure.

Gastrointestinal system:

Nausea, vomiting, abdominal cramping, diarrhea.

Nervous system:

Altered mental status, dizziness, headache, seizures, tearing.

Penatalaksanaan

Airway protection, may include

endotracheal intubation.

Establish an IV of crystalloid

solution.

Pharmacological intervention:

Epinephrine, antihistamines, corticosteroids, vasopressors,

inhaled beta agonists.

Septic Shock
Septic Shock
 An infection that enters the bloodstream and is carried throughout the body.  The toxins
An infection that enters the
bloodstream and is carried
throughout the body.
The toxins released overcome the
compensatory mechanisms.
Can cause the dysfunction of an
organ system or result in multiple
organ dysfunction syndrome.
Tanda & Gejala
Tanda & Gejala
The signs and symptoms are progressive.  Increased to low blood pressure.  High fever, no
The signs and symptoms are
progressive.
Increased to low blood pressure.
High fever, no fever, or hypothermic.
Skin flushed, pale, or cyanotic.
Difficulty breathing and altered lung
sounds.
Altered mental status.
PENATALAKSANAAN
PENATALAKSANAAN
 Airway control.  Support brething if necessary  IV of crystalloid solution.  Dopamine to
Airway control.
Support brething if necessary
IV of crystalloid solution.
Dopamine to support blood
pressure.
Monitor heart rhythm.
KESIMPULAN
KESIMPULAN
 SHOCK ADALAH SYNDROMA KARENA TIDAK ADEKUATNYA PERFUSI JARINGAN SEHINGGA MENGURANGI SUPLAI OKSIGEN DAN NUTRISI YANG
SHOCK ADALAH SYNDROMA KARENA TIDAK
ADEKUATNYA PERFUSI JARINGAN
SEHINGGA MENGURANGI SUPLAI OKSIGEN
DAN NUTRISI YANG DIBUTUHKAN PROSES
METABOLISME TUBUH.
ORGAN TUBUH AKAN BEREAKSI TERHADAP
SHOCK SEBAGAI MEKANISME KOMPENSASI,
BILA GAGAL AKAN TERJADI ISKEMIK
VASKULER, KEGAGALAN FUNGSI ORGAN
DAN AKHIRNYA KEMATIAN

SEMOGA

BERMANFAAT