syok

Recognition, Classification and

Initial Management
 Introduction
 Syok adalah sindrom yang dihasilkan dari pengi
riman oksigen yang tidak memadai untuk meme
nuhi kebutuhan metabolisme
 Oxygen delivery (DO2 ) is less than Oxygen Co
nsumption (< VO2)
 Jika tidak diobati, ini akan menyebabkan asidos
is metabolik, disfungsi organ, dan kematian
Oxygen Delivery
 Oxygen delivery = Cardiac Output x Arterial Oxy
gen Content
(DO2 = CO x CaO2)
 Cardiac Output = Heart Rate x Stroke Volume
(CO = HR x SV)
– SV determined by preload, afterload and contractility
 Arterial Oxygen Content = Oxygen content of the
RBC + the oxygen dissolved in plasma
(CaO2 = Hb X SaO2 X 1.34 + (.003 X PaO2)
Figure 1. FACTORS AFFECTING OXYGEN DELIVERY

Hgb

CaO2
A-a gradient
DPG
Acid-Base Balance
Influenced By Blockers
Oxygenation Competitors
Temperature

DO2
Drugs
Influenced By Conduction System
HR

CVP
CO
EDV Venous Volume
Venous Tone
Metabolic Milieu
SV Ventricular Ions
Compliance Acid Base
Temperature
Influenced By
Drugs
ESV Contractility Toxins

Afterload Blockers
Influenced By Temperature Competitors
Drugs Autonomic Tone
Stadium syok

 Compensated
– Vital organ function maintained, BP remain
s normal.
 Uncompensated
– Microvascular perfusion becomes marginal
. Organ and cellular function deteriorate.
Hypotension develops.
 Irreversible
Clinical Presentation
 Early diagnosis requires a high index
of suspicion

 Diagnosis is made through the physi

cal examination focused on tissue p
erfusion

 Abjecthypotension is a late and pre

morbid sign
 Initial Evaluation: Physical Exa
m Findings of Shock

 Neurological: Fluctuating mental statu

s, sunken fontanel
 Skin and extremities: Cool, pallor, mo
ttling, cyanosis, poor cap refill, weak pu
lses, poor muscle tone.
 Cardio-pulmonary: Hyperpnea, tachy
cardia.
 Renal: Scant, concentrated urine
Initial Evaluation: Directed Hist
ory
 Past medical history
– heart disease

– surgeries

– steroid use

– medical problems

 Brief history of present illness

– exposures

– onset
Differential Diagnosis of Shock
 Cardiogenic
 Hypovolemic  Myocardial dysfunction
 Hemorrhage  Dysrrhythmia
 Fluid loss  Congenital heart disease
 Drugs  Obstructive
 Distributive  Pneumothorax, CardiacTa
 Analphylactic mponade, Aortic Dissecti
on
 Neurogenic
 Septic  Dissociative
 Heat, Carbon monoxide,
Cyanide
 Endocrine
Differential Diagnosis of Shock

 Precise etiologic classification may be del

ayed
 Immediate treatment is essential
 Absolute or relative hypovolemia is usually
present
 Neonate in Shock:
Include in differential:
Congenital adrenal hyperplasia
Inborn errors of metabolism
Obstructive left sided cardiac lesions:
– Aortic stenosis
– Hypoplastic left heart syndrome
– Coarctation of the aorta
– Interrupted aortic arch
Management-General
 Goal: increase oxygen delivery and decr
ease oxygen demand:
 For all children:
○ Oxygen
○ Fluid
○ Temperature control
○ Correct metabolic abnormalities
 Depending on suspected cause:
○ Antibiotics
○ Inotropes
○ Mechanical Ventilation
Management-General

 Airway
 If not protected or unable to be maintained, intubat
e.
 Breathing
 Always give 100% oxygen to start
 Sat monitor
 Circulation
 Establish IV access rapidly
 CR monitor and frequent BP
Management-General

Laboratory studies:
– ABG
– Blood sugar
– Electrolytes
– CBC
– PT/PTT
– Type and cross
– Cultures
Management-Volume Expansion
 Optimize preload
 Normal saline (NS) or lactated ringer’s
(RL)
 Except for myocardial failure use 10-20
ml/kg every 2-10 minutes. Reasses afte
r every bolus.
 At 60ml/kg consider: ongoing losses, adr
enal insufficiency, intestinal ischemia, ob
structive shock. Get CXR. May need ino
tropes.
 Fluid in early septic shock
Carcillo, et al, JAMA, 1991

 Retrospective review of 34 pediatric patients with cul

ture + septic shock, from 1982-1989.
 Hypovolemia determined by PCWP, u.o and hypoten
sion.
 Overall, patients received 33 cc/kg at 1 hour and 95 c
c/kg at 6 hours.
 Three groups:
– 1: received up to 20 cc/kg in 1st 1 hour
– 2: received 20-40 cc/kg in 1st hour
– 3: received greater than 40 cc/kg in 1st hour
 No difference in ARDS between the 3 groups
 Fluid in early septic shock
Carcillo, et al, JAMA, 1991

Group 1 Group 2 Group 3

(n = 14) (n = 11) (n = 9)
Hypovolemic at 6 6 2 0
hours
-Deaths 6 2 0
Not hypovolemic 8 9 9
at 6 hours
-Deaths 2 5 1
Total deaths 8 7 1
Inotropes and Vasopressors
 Lack of history of fluid losses, history of he
art disease, hepatomegaly, rales, cardiom
egaly and failure to improve perfusion with
adequate oxygenation, ventilation, heart r
ate, and volume expansion suggests a car
diogenic or distributive component.
 Consider Appropriate inotropic or vasopre
ssor support.
 Hypovolemic Shock

 Most common form of shock world-wide

 Results in decreased circulating blood v
olume, decrease in preload, decreased
stroke volume and resultant decrease in
cardiac output.
 Etiology: Hemorrhage, renal and/or GI fl
uid losses, capillary leak syndromes
Hypovolemic Shock

 Clinically, history of vomiting/diarrhea or

trauma/blood loss
 Signs of dehydration: dry mucous mem
branes, absent tears, decreased skin tur
gor
 Hypotension, tachycardia without signs
of congestive heart failure
 Hemorrhagic Shock
 Most common cause of shock in the Uni
ted States (due to trauma)
 Patients present with an obvious history
(but in child abuse history may be misle
ading)
 Site of blood loss obvious or concealed
(liver, spleen, intracranial, GI, long bone
fracture)
 Hypotension, tachycardia and pallor
Hypovolemic/Hemorrhagic Sh
ock: Therapy
 Always begin with ABCs
 Replace circulating blood volume rapidl
y: start with crystalloid
 Blood products as soon as available for
hemorrhagic shock (Type and Cross wit
h first blood draw)
 Replace ongoing fluid/blood losses & tre
at the underlying cause
Septic Shock
SIRS/Sepsis/Septic shock

Mediator release:
exogenous & endogenous

Maldistribution Cardiac Imbalance of oxyg Alterations in

en
of blood flow dysfunction metabolism
supply and deman
d
Septic Shock: “Warm Shock”

 Early, compensated, hyperdynamic state

 Clinical signs
 Warm extremities with bounding pulses, tachyca
rdia, tachypnea, confusion.
 Physiologic parameters
 widened pulse pressure, increased cardiac oupt
ut and mixed venous saturation, decreased syst
emic vascular resistance.
 Biochemical evidence:
 Hypocarbia, elevated lactate, hyperglycemia
 Septic Shock: “Cold Shock”
 Late, uncompensated stage with drop in ca
rdiac output.
 Clinical signs
 Cyanosis, cold and clammy skin, rapid thready p
ulses, shallow respirations.
 Physiologic parameters
 Decreased mixed venous sats, cardiac output a
nd CVP, increased SVR, thrombocytopenia, olig
uria, myocardial dysfunction, capillary leak
 Biochemical abnormalities
 Metabolic acidosis, hypoxia, coagulopathy, hypo
glycemia.
Septic Shock
 Cold Shock rapidly progresses to mutiorgan syst
em failure or death if untreated
 Multi-Organ System Failure: Coma, ARDS, CHF,
Renal Failure, Ileus or GI hemorrhage, DIC
 More organ systems involved, worse the progno
sis
 Therapy: ABCs, fluid
 Appropriate antibiotics, treatment of underlying c
ause
Cardiogenic Shock

Etiology:
– Dysrhythmias
– Infection (myocarditis)
– Metabolic
– Obstructive
– Drug intoxication
– Congenital heart disease
– Trauma
Cardiogenic Shock
Differentiation from other types of shock:
– History
– Exam:
 Enlarged liver
 Gallop rhythm
 Murmur
 Rales
– CXR:
 Enlarged heart, pulmonary venous congestion
Cardiogenic Shock
Management:
– Improve cardiac output::
 Correct dysrhthymias
 Optimize preload
 Improve contractility
 Reduce afterload
– Minimize cardiac work:
 Maintain normal temperature
 Sedation
 Intubation and mechanical ventilation
 Correct anemia
Distributive Shock
 Due to an abnormality in vascular tone leadin
g to peripheral pooling of blood with a relative
hypovolemia.
 Etiology
– Anaphylaxis
– Drug toxicity
– Neurologic injury
– Early sepsis
 Management
– Fluid
– Treat underlying cause
Obstructive Shock
 Mechanical obstruction to ventricular outflo
w
 Etiology: Congenital heart disease, massiv
e pulmonary embolism, tension pneumoth
orax, cardiac tamponade
 Inadequate C.O. in the face of adequate pr
eload and contractility
 Treat underlying cause.
Dissociative Shock
 Inability of Hemoglobin molecule to give up
the oxygen to tissues
 Etiology: Carbon Monoxide poisoning, met
hemoglobinemia, dyshemoglobinemias
 Tissue perfusion is adequate, but oxygen r
elease to tissue is abnormal
 Early recognition and treatment of the cau
se is main therapy
Hemodynamic Variables in Diff
erent Shock States
CO SVR MAP Wedge CVP
Hypovolemic    Or   
Cardiogenic    Or   
Obstructive    Or   
Distributive    Or   Or   Or 
Septic: Early    Or   
Septic: Late      or 
Recognition and Classification
Initial Management of Shock
Final Thoughts
 Recognize compensated shock quickly- have a hig
h index of suspicion, remember tachycardia is an
early sign. Hypotension is late and ominous.
 Gain access quickly- if necessary use an intraoseo
us line.
 Fluid, fluid, fluid - Administer adequate amounts of
fluid rapidly. Remember ongoing losses.
 Correct electrolytes and glucose problems quickly.
 If the patient is not responding the way you think h
e should, broaden your differential, think about diff
erent types of shock.
References, Recommended Read
ing, and Acknowledgments
 Uptodate: Initial Management of Shoc
k in Pediatric patients
 Nelson’s Textbook of Pediatrics
 Some slides based on works by Dr. L
ou DeNicola and Dr. Linda Siegel for
PedsCCM
 American Heart Association PALS gui
delines