Diagnosis and Management

of Shock

SHK 1
®
 Shock
• Always a symptom of primary cause
• Inadequate blood flow to meet tissue
oxygen demand
• May be associated with hypotension
• Associated with signs of hypoperfusion:
mental status change, oliguria, acidosis

SHK 2
®
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
sindroma shock

IT IS NOT LOW BLOOD PRESSURE !!!

IT IS HYPOPERFUSION…..
SHK 3
®
 Shock Categories

• Cardiogenic
• Hypovolemic
• Distributive
• Obstructive

SHK 4
®
 Cardiogenic Shock

• Decreased contractility
• Increased filling pressures, decreased
LV stroke work, decreased cardiac
output
• Increased systemic
vascular resistance compensatory

SHK 5
®
 Hypovolemic Shock

• Decreased cardiac output

• Decreased filling pressures
• Compensatory increase in
systemic vascular resistance

SHK 6
®
 Distributive Shock

• Normal or increased cardiac output

• Low systemic vascular resistance
• Low to normal filling pressures
• Sepsis, anaphylaxis, neurogenic,
and acute adrenal insufficiency

SHK
SHK 7
7
®
 Obstructive Shock

• Decreased cardiac output

• Increased systemic vascular
resistance
• Variable filling pressures
dependent on etiology
• Cardiac tamponade, tension
pneumothorax, massive
pulmonary embolus

SHK 8
®
SHK 9
®
 CARDIOGENIC

OBSTRUCTIVE

O2
O2 SEPTIC

O2
HYPOVOLEMIK

SHK 10
®
 Cardiogenic Shock Management

• Treat arrhythmias
• Diastolic dysfunction may
require increased filling
pressures
• Vasodilators if not hypotensive
• Inotrope administration

SHK 11
®
 Cardiogenic Shock Management

• Vasopressor agent needed if

hypotension present to raise
aortic diastolic pressure
• Consultation for mechanical
assist device
• Preload and afterload reduction
to improve hypoxemia if blood
pressure adequate

SHK 12
®
 Hypovolemic Shock
Management
• Volume resuscitation – crystalloid,
colloid
• Initial crystalloid choices
– Lactated Ringer’s solution
– Normal saline (high chloride may
produce hyperchloremic acidosis)
• Match fluid given to fluid lost
– Blood, crystalloid, colloid

SHK
SHK 13
13
®
 Distributive Shock Therapy
• Restore intravascular volume
• Hypotension despite volume therapy
– Inotropes and/or vasopressors
• Vasopressors for MAP < 60 mm Hg
• Adjunctive interventions dependent
on etiology

SHK 14
®
 Obstructive Shock Treatment

• Relieve obstruction
– Pericardiocentesis
– Tube thoracostomy
– Treat pulmonary embolus
• Temporary benefit from fluid
or inotrope administration

SHK 15
®
 Fluid Therapy
• Crystalloids
– Lactated Ringer’s solution
– Normal saline
• Colloids
– Hetastarch
– Albumin
– Gelatins
• Packed red blood cells
• Infuse to physiologic endpoints
SHK
SHK 16
16
®
 Fluid Therapy

• Correct hypotension first

• Decrease heart rate
• Correct hypoperfusion abnormalities
• Monitor for deterioration of
oxygenation

SHK
SHK 17
17
®
 Inotropic / Vasopressor Agents
• Dopamine
– Low dose (2-3 μg/kg/min) – mild inotrope
plus renal effect
– Intermediate dose (4-10 μg/kg/min) –
inotropic effect
– High dose ( >10 μg/kg/min) – vasoconstriction
– Chronotropic effect

SHK
SHK 18
18
®
 Inotropic Agents
• Dobutamine
– 5-20 μg/kg/min
– Inotropic and variable chronotropic effects
– Decrease in systemic vascular resistance

SHK
SHK 19
19
®
 Inotropic / Vasopressor
Agents
• Norepinephrine
– 0.05 μg/kg/min and titrate to effect
– Inotropic and vasopressor effects
– Potent vasopressor at high doses

SHK
SHK 20
20
®
 Inotropic / Vasopressor Agents

• Epinephrine
– Both α and β actions for inotropic and
vasopressor effects
– 0.1 μg/kg/min and titrate
– Increases myocardial O2 consumption

SHK
SHK 21
21
®
 Therapeutic Goals in Shock
• Increase O2 delivery
• Optimize O2 content of blood
• Improve cardiac output and
blood pressure
• Match systemic O2 needs with O2 delivery
• Reverse/prevent organ hypoperfusion

SHK 22
®
 Pediatric Considerations

• BP not good indication of hypoperfusion

• Capillary refill, extremity temperature better
signs of poor systemic perfusion
• Epinephrine preferable to norepinephrine due to
more chronotropic benefit
• Fluid boluses of 20 mL/kg titrated to BP or total
60 mL/kg, before inotropes or vasopressors

SHK
SHK 23
23
®
 Pediatric Considerations
• Neonates – consider congenital
obstructive left heart syndrome as
cause of obstructive shock
• Oliguria
– <2 yrs old, urine volume <2 mL/kg/hr
– Older children, urine volume
<1 mL/kg/hr

SHK
SHK 24
24
®
 How Much Fluid To Give?
■ Some measure of intravascular filling
■ Pressure (CVP or PAOP)
■ Some assessment of risk of pulmonary oedema and
capillary leak
■ Pulmonary gas exchange (PaO2:FiO2)
■ Requirement for positive pressure (PEEP)
■ Chest X-ray
■ Some assessment of response to treatment
■ Changes in acid base balance, lactate
■ Measurement of cardiac output
 What Do You Need to Know When You
Resuscitate a Patient in Shock?
■ Arterial blood pressure
■ Urine output
■ Systemic acid–base balance (pH, SBE, lactate)
■ Some clinical assessment of tissue perfusion
■ “warm and well perfused” or “cold and shut down”
■ Some measurement of global blood flow and tissue perfusion
■ Cardiac output or cardiac index
■ Arterial oxygen delivery, oxygen uptake index
■ Mixed venous saturation and PvO2
 Cardiogenic Distributive
Shock Shock
Inotropes
Vasopressor ( NE,PE,Adr,Dop)
(Dob,Dop,Adr,Amr)

Release Pump = Blood Pressure

P
u

p
=
a

c
s
a

e
r

i
tamponade,etc
Heart
Cardiac Output x
Obstructive SVR
Shock
Volume =
Blood

Hypovolemic
Fluids
Shock
PATOFISIOLOGI DARI RESPON
TUBUH TERHADAP SHOCK

● Respon Neuroendokrin
● Respon Hemodinamik
● Respon Metabolik
 FEAR
Stimulation of limbic Neuroendocrine Respons
area of brain
Adrenal cortex
Increased: Cortisol release
hypothalamic,
adrenomedullary
adrenocortical activity

R atrium Renal
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
 RESPON HEMODINAMIK
Mekanisme untuk memperbaiki keseimbangan
kardiovaskular

● Redistribusi aliran darah

● Peningkatan “cardiac output”

● Memperbaiki volume intravaskular

 RESPON HEMODiNAMiK
REDISTRIBUSI ALIRAN DARAH

HYPOTENSION

STIMULASI NEUROENDOKRIN

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
 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

 HAEMODYNAMIC RESPONSES
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
 RESPON METABOLIK

● Hyperglikemia
● 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 Glycogen
Growth hormone breakdown
Conversion
of a.a. to
glucose
HYPERGLYCEMIA

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

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysis
Pyruvate converted to lactic acid

METABOLIC ACIDOSIS
METABOLIC RESPONS
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
 EFEK SHOCK PADA TINGKATAN SEL

CELL MEMBRANE FAILURE:

• DIRECT
Endotoxin
Complement
• INDIRECT
Failure to maintain normal Na+, K+ or Ca2+ gradient L
Decreased oxidative phosphorylation CELTH
DEA

OSMOTIC
GRADIENT

Na+ entry Water entry CELLULAR IMPAIRED

into cell into cell EDEMA 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
TENSION PNEUMOTHORAX
PRINSIP RESUSITASI

● Mempertahankan ventilasi
● Meningkatkan perfusi
● Terapi penyebab
 MAINTAIN VENTILATION
Increased oxygen
Especially in: demand

Sepsis
Hypovolemia
Trauma Hyperventilation

Diversi blood flow from

Respiratory fatigue
vital organ

Respiratory failure Organ injury

Respiratory acidosis, lethargy-coma, hypoxia
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
 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