SHOCK DAN KONSEP

TERAPI

Yohanes WH George

OBJEKTIF
Memahami peran jantung, status volume
intravaskular dan tahanan pembuluh darah
sistemik dalam mempertahankan tekanan
darah
Belajar mengenai klasifikasi shock
Memahami etiologi dan patogenesis dari shock
Mampu mendiagnosis dan merencanakan
terapi yang adekuat pada masing-masing tipe
shock

DEFINISI
Gangguan dari perfusi jaringan yang terjadi akibat adanya
ketidakseimbangan antara suplai oksigen ke sel dengan
kebutuhan oksigen dari sel tersebut.
Semua jenis shock mengakibatkan gangguan pada perfusi
jaringan yang selanjutnya berkembang menjadi gagal
sirkulasi akut atau disebut juga sindrom shock

IT IS NOT LOW BLOOD PRESSURE

!!!
IT IS HYPOPERFUSION..

TIPE2 SHOCK*
Type

of Shock

Clinical

causes

Hypovolemic

Volume loss

Cardiogenic
Pump failure

Distributive

Obstructive

Increased venous
capacitance or
arteriovenous
shunting
Extra-cardiac
obstruction of blood
flow

Primary

mechanism

Exogenous blood,

plasma, fluid or
electrolyte loss
Myocardial infarction,
cardiac arrhythmias,
heart failure
Septic shock, spinal
shock, autonomic
blockade, drug
overdose
Vena caval
obstruction, cardiac
tamponade,
pulmonary embolism,
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
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
INTRAVASCULAR VOLUME

FAILURE TO MAINTAIN
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

Aorta

Pulmonal
vein

Left
ventricle
Right
ventricle

Left atrium

Blood Pressure

Right
Atrium

Pulmonal artery

Lung

organ

SVR =
Systemic
Vascular
Resistance

PATHOGENESIS OF SHOCK

Cardiogenic
Shock

Distributive
Shock

Inotropes
(Dob,Dop,Adr,Amr)
Release
tamponade,etc

Vasopressor ( NE,PE,ADR,Dop)

Pump =
Heart

Pipe = Vascular

Blood Pressure

Cardiac Output x SVR

Obstructive
Shock
Volume =
Blood

Fluids

Hypovolemic
Shock

PATOFISIOLOGI DARI RESPON

TUBUH TERHADAP SHOCK

Respon Neuroendokrin
Respon Hemodynamik
Respon Metabolic

FEAR

Stimulation of limbic
area of brain

Respon Neuroendokrin

Increased:
hypothalamic,
adrenomedullary
adrenocortical activity

R atrium

low-pressure stretch
receptors
HYPOVOLEMIA

Aorta/carotids
High-pressure
baroreceptors

LOSS OF TONIC
INHIBITION OF
CENTRAL AND
SYMPATHETIC
NERVOUS SYSTEMS

Adrenal cortex
Cortisol release

Renal JGA
Renin release
Pituitary gland
ACTH, ADH and GH release
Adrenal gland (medulla)
Epinephrine/norepinephrine
release

Angiotensin II
Decreased renal
perfusion
Adrenal cortex

Aldosterone release

RESPON HEMODYNAMIC

Mekanisme untuk memperbaiki keseimbangan

kardiovaskular

Redistribusi aliran darah

Peningkatan cardiac output
Memperbaiki volume intravaskular

RESPON HEMODYNAMIK
REDISTRIBUSI ALIRAN DARAH

HYPOTENSION
STIMULASI NEUROENDOKRIN

BLOOD FLOW PROTECTED

Heart
Brain
Adrenal/pituitary gland

BLOOD FLOW DECREASED

Skin
Muscle
Splanchnic circulation

Limited to 180 beats/min

before decreased CO due
to decreased diastolic
filling time

CARDIAC OUTPUT = HR X SV

Increased
contractility
Sympathetic n. system
Catecholamine release

Increase EDV via:

Venoconstriction
Arteriolar constriction
Renal reabsorption

Memperbaiki volume darah

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

RESPON HEMODYNAMIK
Venoconstriction

Sympathetic n. system (SNS)

Catecholamines (CA)
Angiotensin II (ATII)
ADH

Reduced venous
capacitance

Arteriolar constriction
SNS, CA, ATII, ADH

Increased
ventricular
filling P

Decreased capillary P
Fluid shift from interstitium into
vascular compartment

Restoration of
blood volume

SV

Increased distal tubular

reabsorption
Aldosterone, ADH
Increased proximal tubular
reabsorption
SNS, CA, ATII
Increased myocardial
contractility
SNS, CA
Increased heart rate
SNS, CA
Increased SVR due to
arteriolar construction
SNS, CA, ATII, ADH

CO
Increased ventricular
ejection fraction

BP
SVR

RESPON METABOLIK
Hyperglycemia
Mobilisasi lemak
Katabolisme/pemecahan Protein
Peningkatan sintesis urea
Peningkatan asam amino aromatik

Penurunan sintesis reactan fase akut

Peningkatan osmolalitas ekstrasel

RESPON METABOLIK
Release of:
Catecholamines
Cortisol
Glucagon
Growth hormone

HYPERGLYCEMIA
Impaired
peripheral
glucose uptake

Glycogen
breakdown
Conversion
of a.a. to
glucose

Breakdown of
skeletal muscle
into a.a.

RESPON METABOLIK
Decreased blood
volume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysis
Pyruvate converted to lactic acid

METABOLIC ACIDOSIS

RESPON METABOLIK
Release of:
Catecholamines
Cortisol
Glucagon

LIPOLYSIS
INCREASE IN PLASMA FREE
FATTY ACIDS

EFEK SHOCK PADA TINGKATAN SEL

LOW-FLOW,
POOR PERFUSION

HYPOXIA
ACIDOSIS
ANAEROBIC
METABOLISM

DECREASED CELLULAR
ENERGY EFFICIENCY

Glucosebreakdown.(A)Stageone,glycolysis,isanaerobic(does
notrequireoxygen).Ityieldspyruvic acid,withtoxicby-products
suchaslacticacid,andverylittleenergy.(B)Stagetwoisaerobic
(requiresoxygen).InaprocesscalledtheKrebsorcitricacid
cycle,pyruvic acidisdegradedintocarbondioxideandwater,
whichproducesamuchhigheryieldofenergy.

EFEK SHOCK PADA TINGKATAN SEL

CELL MEMBRANE FAILURE:
DIRECT
Endotoxin
Complement
INDIRECT
Failure to maintain normal Na+, K+ or Ca2+ gradient
Decreased oxidative phosphorylation

L
CELTH
DEA

OSMOTIC
GRADIENT

Na+ entry
into cell

Water entry
into cell

CELLULAR
EDEMA

IMPAIRED
INTRACELLULAR
METABOLISM

EFEK SHOCK PADA TINGKATAN

ORGAN
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 STATUS SHOCK

BERDASARKAN PARAMETER
HEMODYNAMIK
TYPE

CVP or
PCWP

Cardiac
Output

SVR

Hypovolemic

Decreased

Decreased

Increased

Cardiogenic

Increased

Decreased

Normal or
Increased

Septic

Increased

Decreased

Traumatic

Decreased or
increased
Decreased

Neurogenic

Decreased

Decreased or Decreased or
increased
increased
Decreased
Decreased

Hypoadrenal

Decreased or
increased

Decreased or Decreased or
increased
increased

TENSION PNEUMOTHORAX

PRINSIP RESUSITASI

Mempertahankan ventilasi
Meningkatkan perfusi
Terapi penyebab

MAINTAIN VENTILATION
Especially in:

Increased oxygen
demand

Sepsis
Hypovolemia
Trauma

Hyperventilation

Respiratory fatigue

Respiratory failure
Respiratory acidosis, lethargy-coma, hypoxia

Diversi blood flow from

vital organ

Organ injury

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
Arterial O2
content

Cardiac
output

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

Inotropes

Fluids

Transfuse

Partially
dependent on
FIO2 and
pulmonary
status

OXYGEN CONSUMPTION / DELIVERY AND SHOCK

VO2 cc/min

DO2/VO2 ratio:
V sat:

2
50

3
66

4
75

5
80

If Sa = 100

240

120

VO2 = Supply Independent

VO2 = Supply dependent

300

600

900

1200

DO2 cc/min

Critical level DO2 in physiological condition = 330 cc/min

Critical level DO2 in pathological condition = 600 cc/min

RESUSCITATION
NEED FOR SPEED

Resuscitation
Fast rate

%
survival

Slow rate
None

Time

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