1、ABCs of Shock,Pediatric Critical Care Medicine Emory University Childrens Healthcare of Atlanta,2,Objectives,Review basic physiology of shock states in pediatrics Classification and recognition of clinical shock states Review initial management of shock,Definition,3,Shock?,4,Shock?,5,6,Definition,Fa
2、ilure of delivery oxygen and substrates to meet the metabolic demands of the tissue beds SUPPLY DEMAND Oxygen delivery Oxygen ConsumptionDO2 VO2 Failure to remove metabolic end-products Result of inadequate blood flow and/or oxygen delivery,7,Definition,Common pathway Failure to deliver substrates c
3、onversion to anaerobic metabolism Reversible if recognized early Irreversible organ damage at the late stage Progressive acidosis and eventually cell death Early recognition is key,8,Epidemiology,Incidence: not clear Shock is not commonly listed as the diagnosis in ER visits Estimated that more chil
4、dren die from sepsis than cancer each year Common causes: hypovolemia, sepsis & trauma Worldwide: diarrhea Developed countries: trauma,9,Pathophysiology,Children Higher % body water Higher resting metabolic rate Higher insensible losses Lower renal concentrating ability Subtle signs/symptoms Higher
5、risk for organ hypo-perfusion,10,Pathophysiology,O2 supply O2 demand O2 delivery O2 consumptionDO2 VO2,11,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 Pa
6、O2) Oxygen content = oxygen carried by HgB + dissolved oxygen,Oxygen delivery (DO2) DO2 = CO x CaO2,12,Critical DO2: consumption depends on delivery,Oxygen delivery DO2 = CO x CaO2,13,Oxygen delivery DO2 = CO x CaO2,CO = HR x SV HR is independent Neonates depend on HR (cant increase SV) SV depends o
7、n 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
8、 strongly affected by PaO2,15,16,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 Increase
9、s adrenergic stress response Increases lipolysis/glycogenolysis (also increases lactate) Releases catecholamine and corticosteroid,Classification of Shock Stages vs. Types,17,18,Stages of Shock,Compensated Maintains end organ perfusion BP is maintained usually by HR Uncompensated Decreases micro-vas
10、cular perfusion Sign/symptoms of end organ dysfunction Hypotensive Irreversible Progressive end-organ dysfunction Cellular acidosis results in cell death,Blood Pressure and Volume,19,BP drops quickly after reaching 50% blood loss CO follows BP closely,20,Systemic Inflammatory Response Syndrome (SIRS
11、),Widespread inflammation due to infection, trauma, burns, etc. Criteria requires 2 of the followings Core temp 38.5C or 10% bands,21,Types of Shock,Hypovolemic Distributive Cardiogenic Septic,Types of Shock,23,Hypovolemic Shock,Most common type in children #1 cause of death worldwide Hemorrhagic: d
12、eveloped 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,24,Hypovolemic Shock,Clinical symptoms Sunken fontanel/eyes Dry mucous membrane
13、Poor skin turgor Delayed capillary refill Cool extremities Tachycardia = compensated shock! Normal BP until volume loss 30-40%,25,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
14、 Loss of vascular tone eventually leads to loss of PRELOAD Blood volume pools in the periphery,26,Distributive Shock,Anaphylaxis is IgE mediated hypersensitive response Massive release of cytokines from activated mast cells Associated with respiratory distress, angioedema, vascular tone collapse Neu
15、rogenic: 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,27,Distributive Shock,Vasodilation Venous poolingDecrease after-loadMal-distribution of regional blood flow,28,Cardioge
16、nic Shock,Impaired CONTRACTILITY (pump failure) 3 categories Cardiomyopathy Arrhythmia Obstruction,29,Cardiogenic Shock,Cardiomyopathy Infectious post viral infection (coxsakie) Infiltrative storage disease Ischemia cardiac arrest or bypass Sepsis late stage,30,Cardiogenic Shock,Arrhythmia Ventricul
17、ar fibrillation & pulseless ventricular tachycardia abolish cardiac output Prolonged or recurrent SVT Brady-arrhythmias or heart block seen in neonatal SLE,31,Cardiogenic Shock,Obstructive Physical obstruction tension pneumothorax, tamponade, pulmonary embolus Congenital - coartation of the aorta, h
18、ypoplastic left heart, critical aortic stenosis Usually present in shock with closing of the ductus arteriosus,Septic Shock,32,33,Septic Shock,20% presentation classic warm shock High CO, low SVR 60% presentation cold shock Low CO, high SVR Small % presentation with mixed pictures,34,Septic Shock,Hi
19、ghest in infants (particularly in newborns) Risks Structural heard disease Neutropenia Neurodevelopmental disorders Invasive devices,Evaluation & Treatment,35,36,Initial Assessment,Goals Immediate identification of life-threatening conditions Rapid recognition of circulatory compromise Early classif
20、ication of the type and cause of shock,37,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,38,Increase O2 contents Increase cardiac out
21、put Increase blood pressure,Early intubation Sedation Analgesia,40,Surviving sepsis Campaign 2008,PALS Shock Algorithm,42,History & Physical Exam,Brief medical history Preceding events, recent illness or trauma PMH Allergies & exposure Focused physical examination Neuro mental status CV HR/perfusion
22、/CR, ?gallop/murmur Resp crackles, wheezing GI - ?HSM,43,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 Menta
23、l status UOP 1 ml/kg/hr,44,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,45,46,Treatment: Volume,Volume resuscitation opti
24、mize 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, MSCarcillo JA, Fields AI. Clinical practice parameters for hemodynamic support of pediatric and neonatal patients in septic shock. Crit. Care
25、Med. 2002; 30:1365-1378,47,Treatment: Volume,Retrospective review of 34 pts with septic shock 266:1242-1245,48,Treatment: Volume,Colloids blood products Trauma or DIC in septic shock PRBC to help with oxygen carrying and delivery,PALS Shock Algorithm,Vasopressors,50,51,Adrenergic Receptors, subtype-
26、1: vascular smooth muscle Increase SVR, afterload Myocardium, bronchial smooth muscle & vessels -1: increase HR & contractility -2: bronchodilation, peripheral vasodilation Dopaminergic renal, coronary, cerebral beds,52,Adrenergic Receptors,Alpha Dopamine BetaEpinephrineNorepinephrine Dobutamine Phe
27、nylephrine?Milrinone,53,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 activity 15 mcg/kg/min activity,54,Dopamine,No evidence to support low-dose (“renal” dose) Evidence that sugges
28、ts dopamine inhibits secretion of prolactin Could increase lymphocyte apoptosis Impairment of immune response to sepsis,55,Norepinephrine,Mostly , minimum to no 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,56
29、,Epinephrine,Mostly with some 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,57,Phenylephrine,Pure activity Significantly increases SVR May have reflex bradycardia Spinal shock,58,Dobutamine,
30、Mainly -1; little -2 and activity Increases contractility & HR increases myocardial oxygen consumption Uses in cardiac patients,59,Milrinone,Phosphodiesterase-3 inhibitor Increases intracellular Ca+ Improves contractility Decreases afterload No increase in myocardial oxygen demand Lusotropic: diasto
31、lic relaxation improve SV Start 0.3 0.5 mcg/kg/min Side effect: hypotension,60,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 vasodilato
32、ry shock 0.01 0.04 U/min,Treatment: Inotropes,61,PALS Shock Algorithm,63,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 c
33、learance: indication of anaerobic metabolism 10% Follow trends,64,Adrenal Insufficiency,Common occurrence in sepsisUse 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,
34、65,Treatment: Steroids,No pediatric study Adult studies hydrocortisone controversy over 28-day mortality International guidelines for management of severe sepsis & septic shock: Surviving Sepsis Campaignhttp:/www.learnicu.org/SiteCollectionDocuments/GuidelineHemodynamicSupport.pdf,66,Summary,Shock i
35、s a dynamic & unstable physiologic state that results in inadequate tissue perfusionHigh morbidity and mortality Tachycardia is the early sign Hypotension is a very late sign Early & aggressive treatment during the “golden hour” improves outcomes,References,Fleegler, E. and M. Kleinman. Guidelines f
36、or pediatric advanced life support. U, 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 manage
37、ment 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. U, last updated Aug 21, 2007. Waltzman, M. Initial management of shock in children. U, last updated May 11, 2010.,
