Diagnosis and

Management
of Shock

SHK 1 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 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…..
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 Shock Categories

• Cardiogenic
• Hypovolemic
• Distributive
• Obstructive

SHK 4 4
®
 Cardiogenic Shock

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

5
 Hypovolemic Shock

• Decreased cardiac output

• Decreased filling pressures
• Compensatory increase in systemic vascular resistance

SHK 6 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 7 7
®
 Obstructive Shock

• Decreased cardiac output

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

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 CARDIOGENIC

OBSTRUCTIVE

O2
O2 SEPTIC

O2
HYPOVOLEMIK

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 Cardiogenic Shock Management

• Treat arrhythmias
• Diastolic dysfunction may require increased filling pressures
• Vasodilators if not hypotensive
• Inotrope administration
• 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
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 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 11 11
®
 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 12 12
®
 Obstructive Shock Treatment
• Relieve obstruction
– Pericardiocentesis
– Tube thoracostomy
– Treat pulmonary embolus
• Temporary benefit from fluid or inotrope administration

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 Fluid Therapy
• Crystalloids
– Lactated Ringer’s solution
– Normal saline
• Colloids
– Hetastarch
– Albumin
– Gelatins
• Packed red blood cells
• Infuse to physiologic endpoints
SHK 14 14
®
 Fluid Therapy
• Correct hypotension first
• Decrease heart rate
• Correct hypoperfusion abnormalities
• Monitor for deterioration of oxygenation

SHK 15 15
®
 Inotropic / Vasopressor Agents

• Dopamine
– Low dose (2-3 g/kg/min) – mild inotrope plus renal effect
– Intermediate dose (4-10 g/kg/min) – inotropic effect
– High dose ( >10 g/kg/min) – vasoconstriction
– Chronotropic effect

SHK 16 16
®
• Dobutamine
– 5-20 g/kg/min
– Inotropic and variable chronotropic effects
– Decrease in systemic vascular resistance

• Norepinephrine
– 0.05 g/kg/min and titrate to effect
– Inotropic and vasopressor effects
– Potent vasopressor at high doses
SHK 17 17
®
 Inotropic / Vasopressor Agents

• Epinephrine
– Both  and  actions for inotropic and
vasopressor effects
– 0.1 g/kg/min and titrate
– Increases myocardial O2 consumption

SHK 18 18
®
 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

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 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
• 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 20 20
®
 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
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 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

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 Cardiogenic Distributive
Shock Shock
Inotropes
Vasopressor ( NE,PE,Adr,Dop)
(Dob,Dop,Adr,Amr)

Release Pump = Pipe = Vascular Blood Pressure

tamponade,etc
Heart

Obstructive Cardiac Output x SVR

Shock
Volume =
Blood

Hypovolemic
Fluids
Shock
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PATOFISIOLOGI DARI RESPON TUBUH
TERHADAP SHOCK

 Respon Neuroendokrin
 Respon Hemodinamik
 Respon Metabolik

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 Neuroendocrine Respons
FEAR
Stimulation of limbic
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 25
 RESPON HEMODINAMIK
Mekanisme untuk memperbaiki keseimbangan
kardiovaskular

 Redistribusi aliran darah

 Peningkatan “cardiac output”

 Memperbaiki volume intravaskular

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 RESPON HEMODiNAMiK
REDISTRIBUSI ALIRAN DARAH

HYPOTENSION

STIMULASI NEUROENDOKRIN

BLOOD FLOW PROTECTED BLOOD FLOW DECREASED

Heart Skin
Brain Muscle
Adrenal/pituitary gland Splanchnic circulation

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 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
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 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

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 HAEMODYNAMIC RESPONSES
Venoconstriction
Sympathetic n. system (SNS)
Catecholamines (CA) Reduced venous
Angiotensin II (ATII) capacitance
ADH

Arteriolar constriction
SNS, CA, ATII, ADH
Increased
ventricular filling
Decreased capillary P 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 30
 RESPON METABOLIK

 Hyperglikemia
 Mobilisasi lemak
 Katabolisme/pemecahan Protein
Peningkatan sintesis urea
Peningkatan asam amino aromatik

 Penurunan sintesis reactan fase akut

 Peningkatan osmolalitas ekstrasel

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 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.
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METABOLIC RESPONS
Decreased blood
volume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysis
Pyruvate converted to lactic acid

METABOLIC ACIDOSIS
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METABOLIC RESPONS
Release of:
Catecholamines
Cortisol
Glucagon

LIPOLYSIS

INCREASE IN PLASMA FREE

FATTY ACIDS

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 EFEK SHOCK PADA TINGKATAN SEL

LOW-FLOW,
POOR PERFUSION

HYPOXIA
ACIDOSIS

ANAEROBIC
METABOLISM

DECREASED CELLULAR
ENERGY EFFICIENCY
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Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does
not require oxygen). It yields pyruvic acid, with toxic by-products
such as lactic acid, and very little energy. (B) Stage two is aerobic
(requires oxygen). In a process called the Krebs or citric acid
cycle, pyruvic acid is degraded into carbon dioxide and water,
which produces a much higher yield of energy.

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 EFEK SHOCK PADA TINGKATAN SEL

CELL MEMBRANE FAILURE:

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

OSMOTIC
GRADIENT

Na+ entry Water entry CELLULAR IMPAIRED

into cell into cell EDEMA INTRACELLULAR
METABOLISM
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 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

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TENSION PNEUMOTHORAX

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PRINSIP RESUSITASI

 Mempertahankan ventilasi
 Meningkatkan perfusi
 Terapi penyebab

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 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

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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
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 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

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 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

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