ABCs of Shock

ABCs of Shock

Pediatric Critical Care MedicineEmory University

Children’s Healthcare of Atlanta

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Objectives• Review basic physiology of shock states in

pediatrics• Classification and recognition of clinical

shock states• Review initial management of shock

Definition

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Shock?

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Shock?

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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

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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

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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

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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

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Pathophysiology

O2 supply < O2 demand

O2 delivery < O2 consumption

DO2 < VO2

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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

Oxygen delivery (DO2)DO2 = CO x CaO2

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Critical DO2: consumption depends on delivery

Oxygen delivery DO2 = CO x CaO2

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• 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

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• 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

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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

Classification of ShockStages vs. Types

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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

Blood Pressure and Volume

% blood loss

% BP

25% Normal

50% 60% o

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•BP drops quickly after reaching 50% blood loss•CO follows BP closely

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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

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

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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

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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%

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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

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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

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Cardiogenic Shock• Impaired CONTRACTILITY (pump failure)• 3 categories

– Cardiomyopathy– Arrhythmia– Obstruction

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Cardiogenic Shock• Cardiomyopathy

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

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Cardiogenic Shock• Arrhythmia

– Ventricular fibrillation & pulseless ventricular tachycardia abolish cardiac output

– Prolonged or recurrent SVT– Brady-arrhythmias or heart block seen in neonatal SLE

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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

Septic Shock

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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

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Septic Shock• Highest in infants (particularly in newborns)• Risks

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

Evaluation & Treatment

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Initial Assessment• Goals

– Immediate identification of life-threatening conditions– Rapid recognition of circulatory compromise– Early classification of the type and cause of shock

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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

Treatment

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Increase O2 contentsIncrease cardiac outputIncrease blood pressure

Early intubationSedationAnalgesia

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Surviving sepsis

Campaign 2008

PALS Shock Algorithm

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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

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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

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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

Volume

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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

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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

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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

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Treatment: Volume

• Colloids – blood products – Trauma or DIC in septic shock– PRBC to help with oxygen carrying and delivery

Vasopressors

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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

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Adrenergic Receptors

Alpha Dopamine Beta

Epinephrine

Norepinephrine DobutaminePhenylephrine

???Milrinone

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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

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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

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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

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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

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Phenylephrine• Pure α activity• Significantly increases SVR

– May have reflex bradycardia

• Spinal shock

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Dobutamine• Mainly β-1; little β-2 and α activity• Increases contractility & HR increases

myocardial oxygen consumption• Uses in cardiac patients

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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

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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

Treatment: Inotropes

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AgentAgent Site of ActionSite of Action DoseDose

Mcg/kg/minMcg/kg/minEffectsEffects

DopamineDopamine DopaminergicDopaminergic

BetaBeta

Alpha > BetaAlpha > Beta

1-31-3

5-105-10

11-2011-20

Renal vasodilationRenal vasodilation

Inotrope/vasoconstrictionInotrope/vasoconstriction

Increase perip. Vasc. Increase perip. Vasc. resistanceresistance

DobutamineDobutamine Beta 1 & 2Beta 1 & 2 1-201-20 InotropeInotrope

VasodilationVasodilation

EpineprhineEpineprhine Beta > alphaBeta > alpha 0.05 – 1.00.05 – 1.0 Inotrope, vasoconstrictionInotrope, vasoconstriction

TachycardiaTachycardia

NorepinephNorepinephrinerine

Alpha > betaAlpha > beta 0.05 – 1.00.05 – 1.0 Profound vasoconstrictionProfound vasoconstriction

inotropeinotrope

MilranoneMilranone PhosphodiesteraPhosphodiesterase inhibitorse inhibitor

0.5 – 0.750.5 – 0.75 InotropeInotrope

vasodilationvasodilation

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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

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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

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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/GuidelineHemodynamicSupport.pdf

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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

References1. 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.

ABCs of Shock

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