Beruflich Dokumente
Kultur Dokumente
WIDODO
Sejarah syok
1960s
1960s
Sejak
Sejak 1905
1905 Sfignomanometer
Sfignomanometer
Syok
=
Hipotensi
Syok = Hipotensi
1970s
1970s
Swan
Swan &
& Ganz
Ganz
Syok
Syok == Hipovolemik,
Hipovolemik, cardiogenik,
cardiogenik, distributif
distributif
1980s
1980s
Teori
Teori supranormal
supranormal value
value (shoemaker),
(shoemaker),
Syok
=
hipoperfusion/
Decrease
Syok = hipoperfusion/ Decrease DO2
DO2 (oxygen
(oxygen delivery)
delivery)
2000s
2000s
SvO2
SvO2 (saturasi
(saturasi mixed
mixed vein),
vein), ditemukan
ditemukan sebagai
sebagai target
target endendpoint
resuscitation
pada
tissue
point resuscitation pada tissue
Syok
Syok == ketidakseimbangan
ketidakseimbangan antara
antara oksigen
oksigen delivery
delivery dan
dan
oksigen
konsumsi
dan
gangguan
pada
mikrosirkulasi
oksigen konsumsi dan gangguan pada mikrosirkulasi
2009-2011s
2009-2011s
Pada
Pada syok,
syok, selain
selain Terjadi
Terjadi hipoperfusi
hipoperfusi (( DO2),
DO2), juga
juga terjadi
terjadi
kerusakan
mitokondria
(seluler
level)
kerusakan mitokondria (seluler level)
Definition of Shock
Inadequate tissue perfusion
Decreased oxygen supply
Anaerobic metabolism
Accumulation metabolic waste
Shock
Life-threatening condition
Immediate or delayed mortality
Multiple aetiology
Pathogenic mechanisms of
shock
Hypovolemic
Hypovolemic
Capillary
leak
SVR
SVR
CO
CO
Microcirculation
Microcirculation
Maldistribution
Maldistribution
Distributive
Distributive
SVR
SVR
CO
CO
Extracardiac
Extracardiac
Obstructive
Obstructive
MAP
MAP
Myocardial
depressan
Inffective
perfusion
SHOCK
Cell Injury
MODS
Coronary
Coronary
perfusion
perfusion
Cardiogenic
Cardiogenic
Signs of Shock
Cold, clammy and pale skin
Rapid, weak, thready pulse
Shallow, rapid breathing
Oliguria
Reduction in MAP
Cyanosis
Loss of consciousness
Level of Consciousness
Report and record
Alert
Verbal response to stimuli
Pain response to stimuli
Unresponsive to any stimuli
Causes of Shock
Severe or sudden blood loss
Large drop in body fluids
Myocardial infarction
Major infections
High spinal injuries
Anaphylaxis
Extreme heat or cold
Types of Shock
Hypovolemic Shock:
haemorrhagic
or non haemorrhagic
Stages of shock
Compensated shock
Autotransfusion
Decompensated shock
Blood moves to more
vital organs
Irreversible shock
Multiple system / organ
damage
Even with treatment, death
is the result
Evaluation of Shock
Internal or external hemorrhage
Underlying cardiac problems
Sepsis
Trauma to spine cord
Contact with known allergic substance
Determine amount of blood loss
How long has casualty been bleeding?
Invasive monitoring
Essential in the definitive treatment
Direct arterial pressure
Central venous pressure
Cardiac output
HR
SV
CVP
PCWP
CO/CI
PR
Spinal Shock
Anaphylaxis
Sepsis
Heart Block
Pump Failure
Relatively
low
Relatively
low
Vol Overload
Inflow obstruction
Outflow obstruction
Hypovolemic
Distributive
Cardiogenic
Treatment of Shock
Increase tissue perfusion and
oxygenation status
Maintain airway
Control bleeding
Baseline vital signs
Level of consciousness
Apakah
Oxygen Delivery
(DO2) ?
Oxygenation PaO2
Carrying capacity
CaO2
SaO2
Haemoglobin
Flow rate
Cardiac Output
Delivery
OXYGEN DELIVERY
(DO2)
Cardiac Output
(CO)
Heart Rate
(HR)
Preload
(SaO2 or SpO2)
Stroke Volume
(SV)
Afterload
Contractility
Hemoglobin
(Hgb)
DO2
Oxygen Delivery
DO2
=
Q (L/min/m2) x
CaO2
(L/min/m2)
DO2 = 3 x (1.34 x Hb x SaO2) x 10
DO2 = 3 x (1.34 x 14 x 0.98) x 10
DO2 = 551 ml/min
(10 dL/L adalah Faktor koreksi, sebab CI dalam L/min/m2 sedangkan CaO 2
in ml/dl)
800
520
1000
720
Cellular use
Oxygenation PaO2
CaO2
DO2
SaO2
Haemoglobin
Flow rate
Cardiac Output
Autoregulation
Distance
Mikrosirkulas
i
Mitochondria
ATP = energy
VO2
Oxygen
consumption/uptake
Oxygen
consumption/uptake
The Fick Equation:
Treatment of Shock
Positioning
ABCD approach
Fluid therapy
Drug therapy
Keep patient at normal temperature
Prevent hypothermia
Minimize effect of shock
Specific measures
Hypovolaemia: Blood transfusion
Electrolyte/acid base imbalance
Sepsis: Antibiotics, ?steroids
Neurogenic: Steroids
Anaphylactic: Adrenalin
Hypovolaemic Shock
Haemorrhage: Overt or occult
Reduction in circulating volume
Reduction in venous return and CO
O2 supply-demand imbalance
Lactic acidosis
Reduction in venous oxygen saturation
Non haemorrhagic hypovolaemia
Severe burns, vomiting and diarrhoea
Clinical Signs
Slightly increased heart rate, local
swelling, bleeding
Increased heart rate, increased diastolic
blood pressure, prolonged capillary refill
30-50
> 50
fld loss)
Control hemorrhage
Restore circulating volume
Optimize oxygen delivery
Vasoconstrictor if BP still low after volume
loading
Non-Haemorrhagic Shock
Cardiogenic Shock
Septic Shock
Neurogenic Shock
Anaphylactic Shock
Cardiogenic Shock
Primary myocardial failure
Arrhythmia
Tamponade
Contusion
Pump failure
Reduction in cardiac output:
Decreased blood supply
Decreased oxygen delivery
Cardiogenic Shock
Assess for:
Signs of heart failure
Signs of tamponade
Cardiac dysrrhythmia
Myocardial infarction
Tachycardia
Muffled heart sounds or third heart sound
Engorged neck veins with hypotension
Dyspnoea
Oedema in feet and ankles
COLLABORATIVE
MANAGEMENT
Treatment is aimed at :
treatment!!!
Optimizing pump by:
Increasing myocardial
O2 delivery
Maximizing CO
Decreasing LV
workload (Afterload)
COLLABORATIVE MANAGEMENT
Limiting/reducing myocardial damage during
Myocardial Infarction:
Increased pumping action & decrease
workload of the heart
Inotropic agents
Vasoactive drugs
Intra-aortic balloon pump
Cautious administration of fluids
Transplantation
Consider thrombolytics, angioplasty in specific cases
Management Cardiogenic
Shock
OPTIMIZING PUMP FUNCTION:
Pulmonary artery monitoring is a necessity !!
Aggressive airway management: Mechanical
Ventilation
Judicious fluid management
Vasoactive agents
Dobutamine
Dopamine
Management Cardiogenic
Shock
OPTIMIZING PUMP FUNCTION (CONT.):
Morphine as needed (Decreases preload,
anxiety)
Cautious use of diuretics in CHF
Vasodilators as needed for afterload reduction
Short acting beta blocker, esmolol, for
refractory tachycardia
Septic Shock
Bacterial, viral, fungal infection
Gram negative and gram positive bacteria
High output failure: warm shock
Fever, tachycardia, tachypnoea, leucocytosis
Cold shock
Atypical presentation in immuno-compromised
patients
Diabetes, Cirrhosis, immunosuppression
Severe Sepsis
Neurogenic Shock
Caused by:
Spinal cord injury
Certain drugs
Brain stem, spinal or torso trauma
Anaphylactic shock
Anafilaksis
Anafilaktoid
(anaphylactoid)
Non immunologic
reaction
Merupakan reaksi anafilaksiis yg tdk
REAKSI
Anafilaksis
Anafilaktoid
Imunologis
Non Imunologis
Lepasnya
Mediators
GEJALANYA SAMA
KEDUANYA KEMATIAN
Anaphylactic Shock
Rapid onset
Primary systems:
Cardiovascular, Respiratory
Skin, Gastrointestinal, coagulation
Face, pharynx and laryngeal oedema
Adrenaline is life saving
Anaphylactic Shock
Diffuse vasodilatation
Increase size of vascular bed
Blood is trapped in small vessels and viscera
Temporary loss in total circulatory volume
Sudden severe allergic reaction to:
Drugs, Toxins, Foods, Plants
Symptoms
Algoritma
penanganan syok
anafilaksis
Terapi
syokdrug
Adrenalin
merupakan
of choice
dari syok
anafilaksis
anafilaksis.
Hal ini disebabkan 3 faktor
yaitu :
Adminsitration Guidelines
for Epinephrine
Mild reactions:
Summary
Life threatening: Early goal directed therapy and regular
monitoring by trained staff will change outcome.
TERIMA
KASIH