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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. Definition. Shock?. Shock?.
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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
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
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
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
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
Pathophysiology O2 supply < O2 demand O2 delivery < O2 consumption DO2 < VO2
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
Critical DO2: consumption depends on delivery Oxygen delivery (DO2)DO2= CO x CaO2
Oxygen delivery DO2= COx 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
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
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
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 • BP drops quickly after reaching 50% blood loss • CO follows BP closely
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
Types of Shock • Hypovolemic • Distributive • Cardiogenic • Septic
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
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%
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
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
Distributive Shock VasodilationVenous pooling Decrease after-load Mal-distribution of regional blood flow
Cardiogenic Shock • Impaired CONTRACTILITY (pump failure) • 3 categories • Cardiomyopathy • Arrhythmia • Obstruction
Cardiogenic Shock • Cardiomyopathy • 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
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 • 20% presentation – classic warm shock • High CO, low SVR • 60% presentation – cold shock • Low CO, high SVR • Small % presentation with mixed pictures
Septic Shock • Highest in infants (particularly in newborns) • Risks • Structural heard disease • Neutropenia • Neurodevelopmental disorders • Invasive devices
Initial Assessment • Goals • Immediate identification of life-threatening conditions • Rapid recognition of circulatory compromise • Early classification of the type and cause of shock
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 Increase O2 contents Increase cardiac output Increase blood pressure Early intubation Sedation Analgesia
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
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
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
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
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
Treatment: Volume • Colloids – blood products • Trauma or DIC in septic shock • PRBC to help with oxygen carrying and delivery