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
2 yr old lethargy,
with temp 34
petechiae C, HR
and flash 180
cap refill 16 yr old
with resp
distress,
muffled
heart
sounds,
distended
neck veins

4
 Shock?

3 month
old with
2 yr old lethargy,
with temp 34
petechia C, HR
e and 180
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

Stroke
Heart Rate
volume

Preload Afterload Contractility

13
 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
– Core temp >38.5˚C or <36˚C
– Tachycardia (or bradycardia in infants)
– Tachypnea
– Elevated or depressed WBC or >10% bands

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 Types of Shock
• Hypovolemic
• Distributive
• Cardiogenic
• Septic

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 Types of Shock
Type Pathophysiology Signs & Symptoms
Hypovolemic ↓ PRELOAD: ↓CO, ↑ SVR, ↑HR, ↓ pulses, delayed cap
intravascular volume loss 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

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 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
– Infectious – post viral infection (coxsakie)
– Infiltrative – storage disease
– Ischemia – cardiac arrest or bypass
– Sepsis – late stage

29
 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

Septic
Sepsis
• Temp instability • Sepsis Shock
• Tachycardia • SIRS • Hypotension • Sepsis
• Tachypnea • Infection • End organ • Hypotension after 40 ml/kg
• WBC ↓ or ↑, (presumed or dysfunction
• Pressor requirement
bands known)
Severe • Further evidence of low
perfusion (lactate, oliguria,
Sepsis AMS)
SIRS

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 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
– Structural heard disease
– Neutropenia
– Neurodevelopmental disorders
– Invasive devices

34
 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 Increase O2
demands delivery

Increase O2 contents Early intubation

Increase cardiac output Sedation
Increase blood pressure Analgesia

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 Surviving sepsis
40 Campaign 2008
PALS Shock Algorithm
 History & Physical Exam
• Brief medical history
– Preceding events, recent illness or trauma
– PMH
– Allergies & exposure
• Focused physical examination
– Neuro – mental status
– CV – HR/perfusion/CR, ?gallop/murmur
– Resp – crackles, wheezing
– GI - ?HSM

42
 Early Goal-Directed Therapy
• Goal – in the first 6 hours of presentation - improvement of
indicators of perfusion and vital organ function
• Physiologic targets
– BP >5th percentile for age
– Quality of central & peripheral pulses
– Normal perfusion
– Mental status
– UOP > 1 ml/kg/hr

43
 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
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

45
 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: up to 20ml/kg
– Group 2: 20-40ml/kg
– Group 3: >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 Dobutamine
Phenylephrine
???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 Site of Action Dose Effects
Mcg/kg/min
Dopamine Dopaminergic 1-3 Renal vasodilation
Beta 5-10 Inotrope/vasoconstriction
Alpha > Beta 11-20 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 0.5 – 0.75 Inotrope
inhibitor vasodilation

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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

• http://www.learnicu.org/SiteCollectionDocuments/GuidelineHemodynamicSupp
ort.pdf

65
 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. Fleegler, E. and M. Kleinman. Guidelines for pediatric advanced life support.
Uptodate.com, last updated Oct 14, 2009.
2. Carcillo, JA et al. Goal-directed management of pediatric shock in the emergency
department. Clinical Pediatric Emergency Medicine: Vol 8; 3; 165-175.
3. 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.
4. 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.
5. McKiernan, CA and SA Lieberman. Circulatory Shock in Children. Pediatrics in Review
2005; 26; 451-460.
6. Pomerantz, W. and M. Roback. Physiology and classification of shock in children.
Uptodate.com, last updated Aug 21, 2007.
7. Waltzman, M. Initial management of shock in children. Uptodate.com, last updated
May 11, 2010.