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Dr Dody Firmanda,SpAn
Dr Dody Firmanda,SpAn

Tatalaksana Syok

dilayanan Primer

Bag. Anestesiologi dan Therapy Intensive Care Fakultas Kedokteran Universitas Islam Sumatera Utara Medan

DEFINISI Gangguan dari perfusi jaringan yang terjadi akibat adanya ketidakseimbangan antara suplai oksigen ke sel
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…
Shock • Always a symptom of primary cause Inadequate blood flow to meet tissue oxygen
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

22/10/2017

mental status change, oliguria, acidosis 22/10/2017 Objectives Define & classify shock Outline management

Objectives

Define & classify shock Outline management principles Discuss goals of fluid resuscitation Understand the concepts of oxygen supply and demand in managing shock. Describe the physiologic effects of vasopressors and inotropic agents

Shock adalah kondisi saat transport oksigen (DO 2 , delivery O 2 ) ke jaringan
Shock adalah kondisi saat transport oksigen (DO 2 ,
delivery O 2 ) ke jaringan gagal memenuhi kebutuhan
metabolik di jaringan tersebut.
“A momentary pause in the act of death.”
-John Collins Warren, 1800s
Types of Shock Cardiogenic (intracardiac vs extracardiac) Hypovolemic Distributive sepsis**** neurogenic (spinal
Types of Shock
Cardiogenic (intracardiac vs extracardiac)
Hypovolemic
Distributive
sepsis****
neurogenic (spinal shock)
adrenal insufficiency
anaphylaxis
Classification of shock states Type of shock Prim ary m echanism Clinical causes Hypovolemic Volume
Classification of shock states
Type of shock
Prim ary m echanism
Clinical causes
Hypovolemic
Volume loss
Exogenous
Blood loss due to hemorrhage
Plasma loss due to burn, inflammation
Fluid and electrolyte loss due to vomiting, diarrhea,
dehydration, osmolal diuresis [diabetes]
Endogenous
Extravasation due to inflammation, trauma, anaphylaxis,
snake venom, pheochromocytoma
Cardiogenic
Pump failure
Myocardial infarction
Heart
failure
Arrhythmia
Intracardiac obstruction
Distributive [vasomotor
dysfunction]
.
High or normal
Expanded venous capacitance
Hypodynamic septic shock due to gram-negative enteric bacillary
resistance
[pooling], CO normal or low
Spinal shock, Narcotic over dose, barbiturate intoxication
.
Low
resistance
Arteriovenous shunting
Pneumonia, peritonitis, abscess, reactive hyperemia
Obstructive
CO normal or high
Extracardiac obstruction of
main channel of blood flow
Vena caval obstruction, pericarditis [cardiac tamponade]
pulmonary embolism, aorta dissecting aneurysm
Weil, MH et al : Cardiovascular System failure. In Principles and practice of
emergency medicine. Schwartz. GR [ed] WB. Saunders 1986
2017/10/22
PATHOPHYSIO, CONT’N Cellular hypoxia / anaerobic metabolism Survival / delayed morbidity / mortality ATP
PATHOPHYSIO, CONT’N
Cellular hypoxia /
anaerobic
metabolism
Survival / delayed
morbidity / mortality
ATP production / lactic acidosis
Intervention / stabilization
Cellular function
impaired
Continued volume loss
Membrane porosity
Lysozymal leakage
Movement of
fluid from
Cellular autodigestion
intravascular to
Irreversible
interstitial spaces
shock
intervention
No. intervention
DEATH
2017/10/22
ATP production fails, the Na + /K + pump fails resulting in the inability to
ATP production fails, the Na + /K + pump fails
resulting in the inability to correct the cell electronic
potential.
Cell swelling occurs leading to rupture and death.
Oxidative Phosphorylation stops & anaerobic
metabolism begins leading to lactic acid
production.

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Approach to various etiologic types of shock Hemorrhagic Cardiogenic Traumatic Septic Sign & Symptoms Sign
Approach to various etiologic types of shock
Hemorrhagic
Cardiogenic
Traumatic
Septic
Sign & Symptoms
Sign & Symptoms
Sign & Symptoms
Sign & Symptoms
Pallor, fainting
Skin clammy , cold
Tachy cardia
Oliguria
Collapse
Pallor, fainting
Skin clammy , cold
Arrhy thmias
Oliguria
Collapse
History
& Phy sical
ev idence of injury
Oliguria
Tachy cardia
Collapse
Fev er, chills
Skin w arm
Tachy cardia
Oliguria
Altered mental status
Collapse
Laboratory
Laboratory
Laboratory
Laboratory
Hct, Hb
Cardiac enzy mes
ECG
X-Ray s, CT-scan
[+] smears & culture
Pathophysiology
Pathophysiology
Pathophysiology
Pathophysiology
Cardiac output
Direct injury
to organ
Peripheral resistance
Blood v olume
Therapy
Therapy
Therapy
Therapy
1. Fluids
1. Antiarrhy thmic
1. Repair injury
1. Antibiotics
2. Blood
2. Vasopressors
2. Fluids
2. Fluids
3. Control Bleeding
3. Vasodilators
3. Blood
3. Drain abscess
Shoemaker, Textbook of Critical Care, third ed. 1995
Pathophysiology ATP + H 2 O ADP + P i + H + + Energy
Pathophysiology
ATP + H 2 O ADP + P i + H + + Energy
Acidosis results from the accumulation of
acid when during anaerobic metabolism
the creation of ATP from ADP is slowed.
H + shift extracellularly and a metabolic
acidosis develops
PRE-LOAD CONTRACTILITY AFTER-LOAD STROKE VOLUME HEART-RATE CARDIAC OUTPUT TOTAL PERIPHERAL RESISTANCE BLOOD
PRE-LOAD
CONTRACTILITY
AFTER-LOAD
STROKE VOLUME
HEART-RATE
CARDIAC OUTPUT
TOTAL PERIPHERAL
RESISTANCE
BLOOD PRESSURE
2017/10/22
CARDIAC OUTPUT • Cardiac output = stroke volume X heart rate • Stroke volume preload,
CARDIAC OUTPUT
• Cardiac output = stroke volume X heart rate
• Stroke volume preload, contractility & afterload
• Venous return (preload) blood volume,posture &venous
tone
• Venous tone control of the sympatheticnervous system
• Venous tone control of the sympatheticnervous system Cardiac Index C.I. = HR x SVI SVI
Cardiac Index C.I. = HR x SVI SVI measures the amount of blood ejected by
Cardiac Index
C.I. = HR x SVI
SVI measures the amount of blood ejected by the ventricle with each
cardiac contraction.
Total blood flow = beats per minute x blood volume ejected per beat

22/10/2017

CARDIAC OUTPUT • Frank–Starling relationship between the left ventricularend-diastolic pressure (LVEDP) and stroke
CARDIAC OUTPUT
• Frank–Starling relationship between the left
ventricularend-diastolic pressure (LVEDP) and
stroke volume (SV)
• The Frank–Starling curve mechanism allows a
ventricle to match its output (stroke volume)to the
volume of blood that enters it (the preload)
Hemodynamic Calculations Parameter Normal Cardiac Index (CI) 2.8 - 4.2 Stroke Volume Index (SVI) 30
Hemodynamic Calculations
Parameter
Normal
Cardiac Index (CI)
2.8 - 4.2
Stroke Volume Index (SVI)
30 - 65
Sys Vasc Resistance Index (SVRI)
1600 - 2400
Left Vent Stroke Work Index (LVSWI) 43 - 62
Vascular Resistance Index SYSTEMIC (SVRI) PULMONARY (PVRI) MAP - CVP x 80 MPAP - PAOP
Vascular Resistance Index
SYSTEMIC (SVRI)
PULMONARY (PVRI)
MAP - CVP
x 80
MPAP - PAOP
x 80
CI
CI
 SVR = vasoconstriction
 SVR = vasodilation
PVR = constriction
PE, hypoxia
Vascular resistance = change in pressure/blood flow
Stroke Work LVSWI = (MAP-PAOP) x SVI x 0.0136 normal = 43 - 62 VSWI
Stroke Work
LVSWI = (MAP-PAOP) x SVI x 0.0136
normal = 43 - 62
VSWI describe how well the ventricles are contracting
and can be used to identify patients who have poor
cardiac function.
ventricular stroke work = pressure x vol. ejected
Rationale for Improving O 2 Delivery Insult Tissue Hypoxia Demands are met Increased Delivery Increased
Rationale for Improving
O 2 Delivery
Insult
Tissue Hypoxia
Demands are met
Increased Delivery
Increased Consumption
Oxygen Calculations • Arterial Oxygen Content (CaO 2 ) • Venous Oxygen Content (CvO 2
Oxygen Calculations
• Arterial Oxygen Content (CaO 2 )
• Venous Oxygen Content (CvO 2 )
Efficiency of the
oxygenation of
• Arteriovenous Oxygen Difference (avDO 2 )
blood and the
rates of oxygen
• Delivery (O 2 AVI)
delivery and
consumption
• Consumption (VO 2 I)

22/10/2017

Definitions • O 2 Delivery - volume of gaseous O 2 delivered to the LV/min.
Definitions
• O 2 Delivery - volume of gaseous O 2 delivered to the
LV/min.
• O 2 Consumption - volume of gaseous O 2 which is
actually used by the tissue/min.
• O 2 Demand - volume of O 2 actually needed by the
tissues to function in an aerobic manner
Demand > consumption = anaerobic metabolism
Critical O 2 Delivery The critical value is variable & is dependent upon the patient,
Critical O 2 Delivery
The critical value is variable
& is dependent upon the patient, disease, and
the metabolic demands of the patient.
DO 2 I
VO 2 I
OXYGEN TRANSPORT DO 2 = CaO 2 x CO VO 2 = [CaO 2 -CvO
OXYGEN TRANSPORT
DO 2 = CaO 2 x CO
VO 2 = [CaO 2 -CvO 2 ] x CO
CaO 2 = SaO 2 x Hb x 1.34
CvO 2 = SvO 2 x Hb x 1.34
SHOCK,
DO 2 < VO 2
2017/10/22
Cardiogenic Shock  Decreased contractility  Increased filling pressures, decreased LV stroke work, decreased
Cardiogenic Shock
 Decreased contractility
 Increased filling pressures, decreased LV stroke work,
decreased cardiac output
 Increased systemic
vascular resistance  compensatory
FEAR Neuroendocrine Respons Stimulation of limbic area of brain Adrenal cortex Increased: Cortisol release
FEAR
Neuroendocrine Respons
Stimulation of limbic
area of brain
Adrenal cortex
Increased:
Cortisol release
hypothalamic,
adrenomedullary
adrenocortical activity
R atrium
Renal
low-pressure stretch
Renin release
receptors
HYPOVOLEMIA
Aorta/carotids
LOSS OF TONIC
INHIBITION OF
CENTRAL AND
SYMPATHETIC
NERVOUS SYSTEMS
Pituitary gland
ACTH, ADH and GH release
High-pressure
Adrenal gland (medulla)
Epinephrine/norepinephrine
release
baroreceptors
Angiotensin II
Decreased renal
perfusion
Adrenal cortex
Aldosterone release
RESPON HEMODiNAMiK REDISTRIBUSI ALIRAN DARAH HYPOTENSION STIMULASI NEUROENDOKRIN BLOOD FLOW PROTECTED Heart Brain
RESPON HEMODiNAMiK
REDISTRIBUSI ALIRAN DARAH
HYPOTENSION
STIMULASI NEUROENDOKRIN
BLOOD FLOW PROTECTED
Heart
Brain
Adrenal/pituitary gland
BLOOD FLOW DECREASED
Skin
Muscle
Splanchnic circulation

22/10/2017

PATOFISIOLOGI DARI RESPON TUBUH TERHADAP SHOCK  Respon Neuroendokrin  Respon Hemodinamik  Respon Metabolik
PATOFISIOLOGI DARI RESPON
TUBUH TERHADAP SHOCK
 Respon Neuroendokrin
 Respon Hemodinamik
 Respon Metabolik
RESPON HEMODINAMIK Mekanisme untuk memperbaiki keseimbangan kardiovaskular  Redistribusi aliran darah 
RESPON HEMODINAMIK
Mekanisme untuk memperbaiki keseimbangan
kardiovaskular
 Redistribusi aliran darah
 Peningkatan “cardiac output”
 Memperbaiki volume intravaskular
Limited to 180 beats/min before decreased CO due to decreased diastolic filling time CARDIAC OUTPUT
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
 Transcapillary refill phase 1. Decreased capillary pressure caused by hypotension 2. Sympathetic increase in
 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 METABOLIK  Hyperglikemia  Mobilisasi lemak  Katabolisme/pemecahan Protein Peningkatan sintesis urea
RESPON METABOLIK
 Hyperglikemia
 Mobilisasi lemak
 Katabolisme/pemecahan Protein
Peningkatan sintesis urea
Peningkatan asam amino aromatik
 Penurunan sintesis reactan fase akut
 Peningkatan osmolalitas ekstrasel
EFEK SHOCK PADA TINGKATAN SEL LOW-FLOW, POOR PERFUSION HYPOXIA ACIDOSIS ANAEROBIC METABOLISM DECREASED CELLULAR
EFEK SHOCK PADA TINGKATAN SEL
LOW-FLOW,
POOR PERFUSION
HYPOXIA
ACIDOSIS
ANAEROBIC
METABOLISM
DECREASED CELLULAR
ENERGY EFFICIENCY

22/10/2017

HAEMODYNAMIC RESPONSES Venoconstriction Sympathetic n. system (SNS) Catecholamines (CA) Angiotensin II (ATII) ADH
HAEMODYNAMIC RESPONSES
Venoconstriction
Sympathetic n. system (SNS)
Catecholamines (CA)
Angiotensin II (ATII)
ADH
Reduced venous
capacitance
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
Aldosterone, ADH
SV
Increased proximal tubular
reabsorption
SNS, CA, ATII
CO
Increased myocardial
Increased ventricular
contractility
ejection fraction
SNS, CA
BP
Increased heart rate
SNS, CA
SVR
Increased SVR due to
arteriolar construction
SNS, CA, ATII, ADH
RESPON METABOLIK Release of: Catecholamines Cortisol Glycogen Glucagon breakdown Growth hormone Conversion of
RESPON METABOLIK
Release of:
Catecholamines
Cortisol
Glycogen
Glucagon
breakdown
Growth hormone
Conversion
of a.a. to
glucose
HYPERGLYCEMIA
Impaired
peripheral
glucose uptake
Breakdown of
skeletal muscle
into a.a.
EFEK SHOCK PADA TINGKATAN SEL CELL MEMBRANE FAILURE: • DIRECT Endotoxin Complement • INDIRECT Failure
EFEK SHOCK PADA TINGKATAN SEL
CELL MEMBRANE FAILURE:
• DIRECT
Endotoxin
Complement
• INDIRECT
Failure to maintain normal Na + , K + or Ca 2+ gradient
Decreased oxidative phosphorylation
OSMOTIC
GRADIENT
IMPAIRED
Na + entry
into cell
Water entry
CELLULAR
INTRACELLULAR
into cell
EDEMA
METABOLISM
EFEK SHOCK PADA TINGKATAN ORGAN  Kidney Oliguric renal failure High output renal failure 
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
MAINTAIN VENTILATION Increased oxygen demand Especially in: Sepsis Hypovolemia Hyperventilation Trauma Respiratory
MAINTAIN VENTILATION
Increased oxygen
demand
Especially in:
Sepsis
Hypovolemia
Hyperventilation
Trauma
Respiratory fatigue
Diversi blood flow from
vital organ
Respiratory failure
Respiratory acidosis, lethargy-coma, hypoxia
Organ injury
TREATMENT CONCEPT OF SHOCK ENHANCING PERFUSION / OXYGEN DELIVERY DO 2 = CO x CaO
TREATMENT CONCEPT OF SHOCK
ENHANCING PERFUSION / OXYGEN DELIVERY
DO 2 = CO x CaO 2
Cardiac
output
Arterial O 2
content
Oxygen delivery/DO 2 = HR X SV X Hb X S0 2 X 1.34 + Hb X paO 2
Inotropes
Transfuse
Partially
Fluids
dependent on
FIO
and
2
pulmonary
status

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PRINSIP RESUSITASI  Mempertahankan ventilasi  Meningkatkan perfusi  Terapi penyebab
PRINSIP RESUSITASI
 Mempertahankan ventilasi
 Meningkatkan perfusi
 Terapi penyebab
TREATMENT OF RESPIRATORY FAILURE Hypovolemia (blood loss) Decreased CO Decreased oxygen delivery, increased oxygen
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
Therapeutic Goals in Shock  Increase O 2 delivery  Optimize O 2 content of
Therapeutic Goals in Shock
 Increase O 2 delivery
 Optimize O 2 content of blood
 Improve cardiac output and
blood pressure
 Match systemic O 2 needs with O 2 delivery
 Reverse/prevent organ hypoperfusion
Cardiogenic Shock Management Treat arrhythmias Diastolic dysfunction may require increased filling pressures
Cardiogenic Shock Management
Treat arrhythmias
Diastolic dysfunction may
require increased filling
pressures
Vasodilators if not hypotensive
Inotrope administration
Fluid Therapy Crystalloids  Lactated Ringer’s solution  Normal saline Colloids  Hetastarch 
Fluid Therapy
Crystalloids
 Lactated Ringer’s solution
 Normal saline
Colloids
 Hetastarch
 Albumin
 Gelatins
Packed red blood cells
Infuse to physiologic endpoints
®
Inotropic / Vasopressor Agents Dopamine  Low dose (2-3 g/kg/min) – mild inotrope plus renal
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
®

22/10/2017

Cardiogenic Shock Management Vasopressor agent needed if hypotension present to raise aortic diastolic pressure
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
Fluid Therapy  Correct hypotension first  Decrease heart rate  Correct hypoperfusion abnormalities 
Fluid Therapy
 Correct hypotension first
 Decrease heart rate
 Correct hypoperfusion abnormalities
 Monitor for deterioration of oxygenation
®
Inotropic Agents  Dobutamine 5-20 g/kg/min Inotropic and variable chronotropic effects Decrease in
Inotropic Agents
 Dobutamine
5-20 g/kg/min
Inotropic and variable chronotropic
effects
Decrease in systemic vascular resistance
®
Inotropic / Vasopressor Agents  Naorepinephrine 0.05 g/kg/min and titrate to effect Inotropic and
Inotropic / Vasopressor Agents
 Naorepinephrine
0.05 g/kg/min and titrate to
effect
Inotropic and vasopressor effects
Potent vasopressor at high doses
®
How Much Fluid To Give?  Some measure of intravascular filling  Pressure (CVP or
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
Cardiogenic Distributive Shock Shock Inotropes Vasopressor ( NE,PE,Adr,Dop) (Dob,Dop,Adr,Amr) Release Pump =
Cardiogenic
Distributive
Shock
Shock
Inotropes
Vasopressor ( NE,PE,Adr,Dop)
(Dob,Dop,Adr,Amr)
Release
Pump =
Blood Pressure
tamponade,etc
Heart
Cardiac Output x SVR
Obstructive
Shock
Volume =
Blood
Hypovolemic
Fluids
Shock
Pipe = Vascular

22/10/2017

Inotropic / Vasopressor Agents  Epinephrine Both  and  actions for inotropic and vasopressor
Inotropic / Vasopressor Agents
 Epinephrine
Both  and  actions for inotropic
and vasopressor effects
0.1 g/kg/min and titrate
Increases myocardial O 2
consumption
®
What Do You Need to Know When You Resuscitate a Patient in Shock?  Arterial
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
SUMMARY  Shock is an altered state of tissue perfusion severe enough to induce derangements
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