ABCs of Shock
Pediatric Critical Care Medicine
Emory University
Children’s Healthcare of Atlanta
Objectives
• Review basic physiology of shock states in
pediatrics
• Classification and recognition of clinical shock
states
• Review initial management of shock
2
Definition
3
Shock?
3 month
old with
lethargy,
temp 34
C, HR
180
2 yr old
with
petechiae
and flash
cap refill 16 yr old
with resp
distress,
muffled
heart
sounds,
distended
neck veins
4
Shock?
3 month
old with
lethargy,
temp 34
C, HR
180
2 yr old
with
petechia
e and
flash cap 16 yr old
refill
with resp
distress,
muffled
heart
sounds,
distended
neck veins
SHOCK
5
Definition
• Failure of delivery oxygen and substrates to meet the
metabolic demands of the tissue beds
SUPPLY < DEMAND
Oxygen delivery < Oxygen Consumption
DO2 < VO2
• Failure to remove metabolic end-products
• Result of inadequate blood flow and/or oxygen delivery
6
Definition
• Common pathway
– Failure to deliver substrates  conversion to anaerobic metabolism
• Reversible if recognized early
• Irreversible organ damage at the late stage
– Progressive acidosis and eventually cell death
• Early recognition is key
7
Epidemiology
• Incidence: not clear
– Shock is not commonly listed as the diagnosis in ER visits
• Estimated that more children die from sepsis than cancer
each year
• Common causes: hypovolemia, sepsis & trauma
– Worldwide: diarrhea
– Developed countries: trauma
8
Pathophysiology
• Children
–
–
–
–
–
Higher % body water
Higher resting metabolic rate
Higher insensible losses
Lower renal concentrating ability
Subtle signs/symptoms
• Higher risk for organ hypo-perfusion
9
Pathophysiology
O2 supply < O2 demand
O2 delivery < O2 consumption
DO2 < VO2
10
Oxygen delivery (DO2)
• DO2 = CO x CaO2
– DO2 : oxygen delivery
– CO : Cardiac output
– CaO2: arterial oxygen content
• CO = HR x SV
– HR: heart rate
– SV: stroke volume
• CaO2 = HgB x SaO2 x 1.34 + (0.003 x PaO2)
– Oxygen content = oxygen carried by HgB + dissolved oxygen
11
Oxygen delivery (DO2)
DO2 = CO x CaO2
Critical DO2: consumption
depends on delivery
12
Oxygen delivery
DO2 = CO x CaO2
Cardiac
Output
13
Heart Rate
Stroke
volume
Preload
Afterload
Contractility
Oxygen delivery
DO2 = CO x CaO2
• CO = HR x SV
• HR is independent
– Neonates depend on HR (can’t increase SV)
• SV depends on
– Pre-load: volume of blood
– After-load: resistance to contraction
– Contractility: force
14
Oxygen delivery
DO2 = CO x CaO2
• CaO2 = HgB x SaO2 x 1.34 + (0.003 x PaO2)
• Normal circumstance: CaO2 is closely associated with SaO2
• Severe anemia or in the presence of abnormal HgB (i.e. CO
poisoning) - CaO2 is strongly affected by PaO2
15
Hypo-perfusion
• Poor perfusion of a vital organs leads to organ dysfunction
– Decreased urine output
– Altered mental status
– Elevated LFTs, bilirubin
• Switches to anaerobic metabolism  Lactate
• Activates inflammatory cascade
– Activates neutrophils, releases cytokines
• Increases adrenergic stress response
– Increases lipolysis/glycogenolysis (also increases lactate)
– Releases catecholamine and corticosteroid
16
Classification of Shock
Stages vs. Types
17
Stages of Shock
• Compensated
– Maintains end organ perfusion
– BP is maintained usually by ↑ HR
• Uncompensated
– Decreases micro-vascular perfusion
– Sign/symptoms of end organ dysfunction
– Hypotensive
• Irreversible
– Progressive end-organ dysfunction
– Cellular acidosis results in cell death
18
Blood Pressure and Volume
% blood loss
% BP
25%
Normal
50%
60% o
•BP drops quickly after
reaching 50% blood loss
•CO follows BP closely
19
Systemic Inflammatory Response
Syndrome (SIRS)
• Widespread inflammation due to infection, trauma, burns,
etc.
• Criteria – requires 2 of the followings
–
–
–
–
20
Core temp >38.5˚C or <36˚C
Tachycardia (or bradycardia in infants)
Tachypnea
Elevated or depressed WBC or >10% bands
Types of Shock
•
•
•
•
21
Hypovolemic
Distributive
Cardiogenic
Septic
Types of Shock
Type
Pathophysiology
Signs & Symptoms
Hypovolemic
↓ PRELOAD: ↓CO, ↑ SVR,
intravascular volume loss
↑HR, ↓ pulses, delayed cap
refill, dry skin, sunken eyes,
oliguria
Distributive
↓ AFTERLOAD (SVR)
Anaphylactic
↑ CO, ↓ SVR
Angioedema, low BP,
wheezing, resp. distress
Spinal
Normal CO, ↓ SVR
Low BP without tachycardia;
paralysis, h/o trauma
Cardiogenic
↓ CO, variable SVR
Normal to ↑ HR, ↓ pulses,
delayed CR, JVD, murmur or
gallop, hepatomegaly
Septic
Variable
More to come
Hypovolemic Shock
• Most common type in children
• #1 cause of death worldwide
– Hemorrhagic: developed countries – GI bleed, trauma (liver/spleen
injuries, long bone fractures), intracranial hemorrhage
– Non-hemorrhagic: vomiting/diarrhea, heat stroke, burns, DKA
• Pathophysiology:
– Loss of intravascular volume  ↓ PRELOAD
23
Hypovolemic Shock
• Clinical symptoms
–
–
–
–
–
Sunken fontanel/eyes
Dry mucous membrane
Poor skin turgor
Delayed capillary refill
Cool extremities
• Tachycardia = compensated shock!
– Normal BP until volume loss >30-40%
24
Distributive Shock
• Loss of SVR (AFTERLOAD) results in abnormal
distribution of blood flow
• Increased CO and HR
– Often hyper dynamic contractility, bounding pulses, flash CR
• Loss of vascular tone eventually leads to loss of PRELOAD
– Blood volume pools in the periphery
25
Distributive Shock
• Anaphylaxis is IgE mediated hypersensitive response
– Massive release of cytokines from activated mast cells
– Associated with respiratory distress, angioedema, vascular tone
collapse
• Neurogenic: unusual and mostly transient
– Follows acute CNS injury (brain or spinal cord)
– Loss of sympathetic and autonomic tone
– Unique presentation: hypotension with normal heart rate
26
Distributive Shock
Vasodilation
Venous pooling
Decrease after-load
Mal-distribution of regional blood flow
27
Cardiogenic Shock
• Impaired CONTRACTILITY (pump failure)
• 3 categories
– Cardiomyopathy
– Arrhythmia
– Obstruction
28
Cardiogenic Shock
• Cardiomyopathy
–
–
–
–
29
Infectious – post viral infection (coxsakie)
Infiltrative – storage disease
Ischemia – cardiac arrest or bypass
Sepsis – late stage
Cardiogenic Shock
• Arrhythmia
– Ventricular fibrillation & pulseless ventricular tachycardia abolish
cardiac output
– Prolonged or recurrent SVT
– Brady-arrhythmias or heart block seen in neonatal SLE
30
Cardiogenic Shock
• Obstructive
– Physical obstruction – tension pneumothorax, tamponade,
pulmonary embolus
– Congenital - coartation of the aorta, hypoplastic left heart, critical
aortic stenosis
» Usually present in shock with closing of the ductus arteriosus
31
Septic Shock
•
•
•
•
Temp instability
Tachycardia
Tachypnea
WBC ↓ or ↑,
bands
SIRS
32
Septic
Shock
Sepsis
• SIRS
• Infection
(presumed or
known)
• Sepsis
• Hypotension
• End organ
dysfunction
Severe
Sepsis
•
•
•
•
Sepsis
Hypotension after 40 ml/kg
Pressor requirement
Further evidence of low
perfusion (lactate, oliguria,
AMS)
Septic Shock
• 20% presentation – classic warm shock
– High CO, low SVR
• 60% presentation – cold shock
– Low CO, high SVR
• Small % presentation with mixed pictures
33
Septic Shock
• Highest in infants (particularly in newborns)
• Risks
–
–
–
–
34
Structural heard disease
Neutropenia
Neurodevelopmental disorders
Invasive devices
Evaluation & Treatment
35
Initial Assessment
• Goals
– Immediate identification of life-threatening conditions
– Rapid recognition of circulatory compromise
– Early classification of the type and cause of shock
36
Initial Assessment
• Airway
– Mental status: can the patient maintain the airway
• Breathing
– ?impending respiratory failure
• Circulation
– Heart rate, pulses, blood pressure
– Capillary refills - perfusion
• Dextrose
37
Treatment
Decrease O2
demands
Increase O2 contents
Increase cardiac output
Increase blood pressure
38
Increase O2
delivery
Early intubation
Sedation
Analgesia
40
Surviving sepsis
Campaign 2008
PALS Shock Algorithm
History & Physical Exam
• Brief medical history
– Preceding events, recent illness or trauma
– PMH
– Allergies & exposure
• Focused physical examination
–
–
–
–
42
Neuro – mental status
CV – HR/perfusion/CR, ?gallop/murmur
Resp – crackles, wheezing
GI - ?HSM
Early Goal-Directed Therapy
• Goal – in the first 6 hours of presentation - improvement of
indicators of perfusion and vital organ function
• Physiologic targets
–
–
–
–
–
43
BP >5th percentile for age
Quality of central & peripheral pulses
Normal perfusion
Mental status
UOP > 1 ml/kg/hr
Fluid Resuscitation
• Isotonic crystalloids – availability
– 20cc/kg  reassess (overload vs. third spacing)
• Rapid infusion – 5 - 10 min
• NO upper limit
– Pressor if > 60ml/kg
– May need up to 100-200 ml/kg during the first few hours
44
Volume
45
LR
NS
pH
6.0-7.5
4.5-7.0
Na+
130
154
K+
4
0
Ca++
3
0
Cl-
109
154
Lactate
28
0
Calorie
9
0
Osmolarity
273
308
Treatment: Volume
• Volume resuscitation  optimize preload
• >60 ml/kg during 1st hr associated with increase survival
• Titrate volume to improve CO, normal HR, BP; improve
perfusion/cap refill; improve UOP, MS
– Carcillo JA, Fields AI. Clinical practice parameters for hemodynamic
support of pediatric and neonatal patients in septic shock. Crit. Care
Med. 2002; 30:1365-1378
46
Treatment: Volume
• Retrospective review of 34 pts with septic shock &
hypovolemia with 1st hr fluid resuscitation
– Group 1:
– Group 2:
– Group 3:
up to 20ml/kg
20-40ml/kg
>40mg/kg
• No different in rate of ARDS
– Carcillo JA, Davis AL, Zaritsky A, Role of early fluid resuscitation in
pediatric septic shock. JAMA. 1991; 266:1242-1245
47
Treatment: Volume
• Colloids – blood products
– Trauma or DIC in septic shock
– PRBC to help with oxygen carrying and delivery
48
PALS Shock Algorithm
Vasopressors
50
Adrenergic Receptors
• α – subtype-1: vascular smooth muscle
– Increase SVR, afterload
• β – Myocardium, bronchial smooth muscle & vessels
– β -1: increase HR & contractility
– β -2: bronchodilation, peripheral vasodilation
• Dopaminergic – renal, coronary, cerebral beds
51
Adrenergic Receptors
Alpha
Dopamine
Beta
Epinephrine
Norepinephrine
Phenylephrine
Dobutamine
???Milrinone
52
Dopamine
•
•
•
•
Readily available, pre-mixed
PIV up to 10 mcg/kg/min
Start at 5 mcg/kg/min, titrate to effects
Receptors
– 2-5 mcg/kg/min (renal) – D receptors
– 5-15 mcg/kg/min – β activity
– >15 mcg/kg/min – α activity
53
Dopamine
• No evidence to support low-dose (“renal” dose)
• Evidence that suggests dopamine inhibits secretion of
prolactin
– Could increase lymphocyte apoptosis
– Impairment of immune response to sepsis
54
Norepinephrine
• Mostly α, minimum to no β activity  increase SVR and
after-load
• Start at 0.05 – 0.1 mcg/kg/min (max 1 mcg/kg/min)
• “Warm” septic shock
• Avoid in myocardial dysfunction
55
Epinephrine
• Mostly β with some α activity
• Start at 0.05 – 0.1 mcg/kg/min (max 1 mcg/kg/min)
• “Cold” septic shock
– Improves contractility + vasoconstriction
– Best drug for myocardial dysfunction
56
Phenylephrine
• Pure α activity
• Significantly increases SVR
– May have reflex bradycardia
• Spinal shock
57
Dobutamine
• Mainly β-1; little β-2 and α activity
• Increases contractility & HR  increases myocardial
oxygen consumption
• Uses in cardiac patients
58
Milrinone
• Phosphodiesterase-3 inhibitor
• Increases intracellular Ca++
– Improves contractility
– Decreases afterload
– No increase in myocardial oxygen demand
– Lusotropic: diastolic relaxation  improve SV
• Start 0.3 – 0.5 mcg/kg/min
• Side effect: hypotension
59
Vasopressin
• V-2 receptor:
– Vasoconstriction mainly in the capillaries and small arterioles
– Direct stimulation to pituitary gland  ACTH production
– Restores catecholamine sensitivity
• Uses in catecholamine-resistant vasodilatory shock
• 0.01 – 0.04 U/min
60
Treatment: Inotropes
Agent
61
Site of Action
Dose
Mcg/kg/min
Effects
Dopamine
Dopaminergic
Beta
Alpha > Beta
1-3
5-10
11-20
Renal vasodilation
Inotrope/vasoconstriction
Increase perip. Vasc. resistance
Dobutamine
Beta 1 & 2
1-20
Inotrope
Vasodilation
Epineprhine
Beta > alpha
0.05 – 1.0
Inotrope, vasoconstriction
Tachycardia
Norepinephrine
Alpha > beta
0.05 – 1.0
Profound vasoconstriction
inotrope
Milranone
Phosphodiesterase
inhibitor
0.5 – 0.75
Inotrope
vasodilation
PALS Shock Algorithm
Therapy Monitoring
• Central venous pressure
– Intravascular volume
– Goal 6 mmgHg (nl 4-8 mmHg)
• Mixed venous saturation (SvO2)
– Goal >70% (nl 65-70%)
– Indicate oxygen extraction by the tissues
– Best obtained from CVL: SC or IJ
• Lactate clearance: indication of anaerobic metabolism
– >10%
– Follow trends
63
Adrenal Insufficiency
• Common occurrence in sepsis
– Use of Etomidate for intubation
– Chronic steroid use
• 2 forms of insufficiency
– Absolute: random cortisol <10
– Relative: ∆ <9
• Tx: Hydrocortisone
– Load: 100mg/m2
– Maintenance: 25mg/m2 Q6 x 7 days
64
Treatment: Steroids
• No pediatric study
• Adult studies – hydrocortisone controversy over 28-day
mortality
• International guidelines for management of severe sepsis &
septic shock: Surviving Sepsis Campaign
•
65
http://www.learnicu.org/SiteCollectionDocuments/GuidelineHemodynamicSupp
ort.pdf
Summary
• Shock is a dynamic & unstable physiologic state that results
in inadequate tissue perfusion
– High morbidity and mortality
• Tachycardia is the early sign
• Hypotension is a very late sign
• Early & aggressive treatment during the “golden hour”
improves outcomes
66
References
1.
2.
3.
4.
5.
6.
7.
Fleegler, E. and M. Kleinman. Guidelines for pediatric advanced life support.
Uptodate.com, last updated Oct 14, 2009.
Carcillo, JA et al. Goal-directed management of pediatric shock in the emergency
department. Clinical Pediatric Emergency Medicine: Vol 8; 3; 165-175.
Dellinger, RP et al. Surviving Sepsis Campaign: international guidelines for
management of severe sepsis and septic shock: 2008. Intensive Care Medicine: Vol 34; 1;
17-60.
Han, YY et al. Early reversal of pediatric-neonatal septic shock by community
physicians is associated with improved outcome. Pediatrics: Vol 112; 4; 793-799.
McKiernan, CA and SA Lieberman. Circulatory Shock in Children. Pediatrics in Review
2005; 26; 451-460.
Pomerantz, W. and M. Roback. Physiology and classification of shock in children.
Uptodate.com, last updated Aug 21, 2007.
Waltzman, M. Initial management of shock in children. Uptodate.com, last updated
May 11, 2010.