shock avni m. bhalakia, m.d. st. barnabas hospital

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Shock Shock Avni M. Bhalakia, M.D. Avni M. Bhalakia, M.D. St. Barnabas Hospital St. Barnabas Hospital

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Page 1: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

ShockShock

Avni M. Bhalakia, M.D.Avni M. Bhalakia, M.D.

St. Barnabas HospitalSt. Barnabas Hospital

Page 2: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Learning ObjectivesLearning Objectives

Define shock, understand the Define shock, understand the pathophysiology & the stagespathophysiology & the stages

Identify the major categories of Identify the major categories of shock & their typical presentationshock & their typical presentation

Know the initial steps of evaluation Know the initial steps of evaluation and management in shockand management in shock

Know the goals of fluid resuscitationKnow the goals of fluid resuscitation

Page 3: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

ShockShock

Defined as a physiologic state of Defined as a physiologic state of circulatory dysfunction that leads to circulatory dysfunction that leads to inadequate oxygen delivery or utilization inadequate oxygen delivery or utilization to meet the metabolic demands of cellsto meet the metabolic demands of cells

Influenced by Influenced by Insufficient intravascular volume (preload)Insufficient intravascular volume (preload) Changes in vascular resistance (afterload)Changes in vascular resistance (afterload) Cardiac dysfunction (poor cardiac output)Cardiac dysfunction (poor cardiac output) Obstruction to blood flowObstruction to blood flow

Page 4: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

PathophysiologyPathophysiology

Shock = oxygen demand > supplyShock = oxygen demand > supply Shock is inadequate perfusion to meet Shock is inadequate perfusion to meet

metabolic demands of tissues metabolic demands of tissues relates to relates to oxygen deliveryoxygen delivery

Oxygen delivery = CO x arterial oxygen contentOxygen delivery = CO x arterial oxygen content Arterial oxygen content depends on hemoglobin Arterial oxygen content depends on hemoglobin

concentration (oxygen carrying capacity) and the concentration (oxygen carrying capacity) and the percentage of blood carrying oxygen (oxygen percentage of blood carrying oxygen (oxygen saturation)saturation)

CO depends on HR x SVCO depends on HR x SV SV depends on preload, afterload, and contractilitySV depends on preload, afterload, and contractility

Page 5: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Stages of ShockStages of Shock

CompensatedCompensated DecompensatedDecompensated IrreversibleIrreversible

States of shock can overlapStates of shock can overlap

Page 6: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Compensated ShockCompensated Shock

Body compensates for states of diminished Body compensates for states of diminished perfusion and reduced oxygen delivery (supply perfusion and reduced oxygen delivery (supply and demand are in balance)and demand are in balance)

Normal blood pressure is maintained Normal blood pressure is maintained TachycardiaTachycardia VasoconstrictionVasoconstriction decreased peripheral decreased peripheral

perfusionperfusion Cool extremitiesCool extremities Prolonged capillary refillProlonged capillary refill Decreased peripheral pulsesDecreased peripheral pulses OliguriaOliguria

Page 7: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Decompensated ShockDecompensated Shock

LATE finding in pediatric patientsLATE finding in pediatric patients Body’s compensatory mechanisms are Body’s compensatory mechanisms are

overwhelmed and fail (demand exceeds supply)overwhelmed and fail (demand exceeds supply) HypotensionHypotension Signs & symptoms of end-organ dysfunctionSigns & symptoms of end-organ dysfunction

Depressed mental statusDepressed mental status AnuriaAnuria Metabolic acidosisMetabolic acidosis TachypneaTachypnea Weak central pulsesWeak central pulses

Page 8: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Irreversible StageIrreversible Stage

End organ dysfunction leads to end-End organ dysfunction leads to end-organ death which is irreversible organ death which is irreversible despite resuscitative efforts despite resuscitative efforts

Page 9: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Types of ShockTypes of Shock

Hypovolemic shock: decreased Hypovolemic shock: decreased preloadpreload

Cardiogenic shock: pump failureCardiogenic shock: pump failure Distributive shock: not enough Distributive shock: not enough

volume for available spacevolume for available space Obstructive shockObstructive shock

Page 10: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Hypovolemic ShockHypovolemic Shock

Most common type of shock in childrenMost common type of shock in children EtiologyEtiology

Fluid loss or inadequate intakeFluid loss or inadequate intake Vomiting, Diarrhea, Excessive SweatingVomiting, Diarrhea, Excessive Sweating

HemorrhageHemorrhage Trauma, GITrauma, GI

Vascular Leak SyndromeVascular Leak Syndrome Sepsis/SIRS, BurnsSepsis/SIRS, Burns

Page 11: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Hypovolemic ShockHypovolemic Shock

Physical exam reflects the degree of Physical exam reflects the degree of volume depletionvolume depletion EarlyEarly: ↑ HR and ↓ perfusion with narrow : ↑ HR and ↓ perfusion with narrow

pulse widthpulse width LateLate: ↑↑ HR, ↓↓ perfusion and ↓ BP with : ↑↑ HR, ↓↓ perfusion and ↓ BP with

end organ dysfunctionend organ dysfunction Cool extremities, poor peripheral pulses, Cool extremities, poor peripheral pulses,

prolonged capillary refill, dry mucous prolonged capillary refill, dry mucous membrances, tachycardia, tachypneamembrances, tachycardia, tachypnea

Page 12: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Cardiogenic ShockCardiogenic Shock

Acute hypo-perfusion and acidosis due to Acute hypo-perfusion and acidosis due to heart failureheart failure

History usually more subtleHistory usually more subtle Cough, poor weight gain, fatigueCough, poor weight gain, fatigue

EtiologyEtiology ArrhythmiasArrhythmias Infectious or immunologic disordersInfectious or immunologic disorders IschemiaIschemia Congenital & structural heart diseaseCongenital & structural heart disease CardiomyopathiesCardiomyopathies

Page 13: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Cardiogenic ShockCardiogenic Shock

Physical exam findings depend on which Physical exam findings depend on which ventricle is in failureventricle is in failure LV dysfunction: pulmonary edemaLV dysfunction: pulmonary edema RV dysfuntion: hepato/splenomegalyRV dysfuntion: hepato/splenomegaly Cool extremities, prolonged cap refill, poor Cool extremities, prolonged cap refill, poor

peripheral pulses, tachycardiaperipheral pulses, tachycardia Chest X-ray shows cardiomegaly and Chest X-ray shows cardiomegaly and

pulmonary edemapulmonary edema Evaluate with emergent echocardiogram to Evaluate with emergent echocardiogram to

look at anatomy, systolic and diastolic functionlook at anatomy, systolic and diastolic function

Page 14: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Distributive ShockDistributive Shock

Loss of sympathetic activity and vascular Loss of sympathetic activity and vascular tone tone maldistribution of blood flow maldistribution of blood flow relative hypovolemia and hypotensionrelative hypovolemia and hypotension

History of high fevers, head or spinal History of high fevers, head or spinal injury, major abdominal surgery (third-injury, major abdominal surgery (third-spacing)spacing)

EtiologyEtiology AnaphylaxisAnaphylaxis Spinal Cord InjuriesSpinal Cord Injuries Cortisol-deficient statesCortisol-deficient states Septic shock Septic shock

Page 15: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Distributive ShockDistributive Shock

Reduced peripheral vascular tone Reduced peripheral vascular tone leads to pooling of blood in leads to pooling of blood in extremities extremities poor venous return poor venous return

Physical exam depends on stagePhysical exam depends on stage Early: Warm extremities, wide pulse Early: Warm extremities, wide pulse

pressure, low diastolic pressurepressure, low diastolic pressure Late: perfusion pressure falls and Late: perfusion pressure falls and

acidosis developsacidosis develops

Page 16: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Bacteremia, SIRS, SepsisBacteremia, SIRS, Sepsis

BacteremiaBacteremia: an identifiable organism : an identifiable organism cultured from the bloodcultured from the blood

Systemic Inflammatory Response Systemic Inflammatory Response Syndrome (SIRS)Syndrome (SIRS): sepsis without organism : sepsis without organism identified. Meet at least 2 of criteria:identified. Meet at least 2 of criteria: Hypo or hyperthermiaHypo or hyperthermia Tachycardia or bradycardiaTachycardia or bradycardia Tachypnea Tachypnea Leukocytosis or leukopeniaLeukocytosis or leukopenia

SepsisSepsis: SIRS from a systemic illness : SIRS from a systemic illness (bacterial, viral, protozoal)(bacterial, viral, protozoal)

Page 17: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Septic ShockSeptic Shock

Sepsis + cardiovascular dysfunctionSepsis + cardiovascular dysfunction Results from the direct effect of Results from the direct effect of

microorganism and its toxinsmicroorganism and its toxins Usually bacteria: Gram negative more often Usually bacteria: Gram negative more often

than Gram (+) bacteria, viruses can cause than Gram (+) bacteria, viruses can cause septic shockseptic shock

Most frequently occurs in Most frequently occurs in immunosuppressed or young individuals but immunosuppressed or young individuals but can effect anyone (i.e., meningococcemia) can effect anyone (i.e., meningococcemia)

Page 18: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Pathophysiology of Septic Pathophysiology of Septic ShockShock

Invading microorganism leads to Invading microorganism leads to inflammation, cytokine release, inflammation, cytokine release, endothelial activation, nitric oxide endothelial activation, nitric oxide release, and activation of coagulation release, and activation of coagulation cascadecascade VasodilatationVasodilatation Capillary integrity compromisedCapillary integrity compromised Depressed myocardial function and Depressed myocardial function and

reduced cardiac contractilityreduced cardiac contractility

Page 19: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Septic ShockSeptic Shock

Early “Warm Early “Warm Shock”Shock”

↑ ↑ CO and ↓ SVR and CO and ↓ SVR and wide pulse pressurewide pulse pressure

Signs: warm Signs: warm extremities, flushing, extremities, flushing, bounding pulses, ↑ bounding pulses, ↑ HR, confusionHR, confusion

Hypocarbia, elevated Hypocarbia, elevated lactate, lactate, hyperglycemiahyperglycemia

Late “Cold Shock”Late “Cold Shock” Uncompensated Uncompensated

shock with drop in COshock with drop in CO Signs: cyanosis, cold, Signs: cyanosis, cold,

clammy skin, thready clammy skin, thready pulse, shallow pulse, shallow respirationrespiration

Metabolic acidosis, Metabolic acidosis, hypoxia, hypoxia, coagulopathy, coagulopathy, hypoglycemiahypoglycemia

Page 20: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Obstructive ShockObstructive Shock

Obstruction of blood flow from heart to Obstruction of blood flow from heart to tissues (low CO despite normal tissues (low CO despite normal intravascular volume and myocardial intravascular volume and myocardial function)function) Congenital causes such as ductus Congenital causes such as ductus

arterious closesarterious closes Acquired causes such as hypertrophic Acquired causes such as hypertrophic

cardiomyopathy, valvular disease, cardiac cardiomyopathy, valvular disease, cardiac tamponadetamponade

Page 21: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

ShockShock

DiagnosisDiagnosis Clinical AssessmentClinical Assessment Laboratory EvaluationLaboratory Evaluation ManagementManagement

Page 22: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Diagnose ShockDiagnose Shock

Early recognition is keyEarly recognition is key High index of suspicionHigh index of suspicion

Clinical assessment & evidence of Clinical assessment & evidence of inadequate perfusioninadequate perfusion

Page 23: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Clinical AssessmentClinical Assessment

Vital signsVital signs Pulse oximetry, heart rate, blood pressurePulse oximetry, heart rate, blood pressure

Serial physical examsSerial physical exams Neuro: Waxing and waning mental status Neuro: Waxing and waning mental status Cardiopulmonary: Hyperpnea, tachycardiaCardiopulmonary: Hyperpnea, tachycardia Renal: Scant, concentrated urine or AnuriaRenal: Scant, concentrated urine or Anuria Skin and extremities: Cool, pallor, mottling, Skin and extremities: Cool, pallor, mottling,

cyanosis, poor cap refill, weak pulses, poor cyanosis, poor cap refill, weak pulses, poor muscle tone, sunken fontanelle muscle tone, sunken fontanelle

Page 24: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Hypotension is a late Hypotension is a late and pre-morbid and pre-morbid

signsign

Page 25: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Laboratory EvaluationLaboratory Evaluation

Arterial blood gasArterial blood gas Serum glucose (CBG)Serum glucose (CBG) Electrolytes (include Electrolytes (include

serum ionized serum ionized calcium)calcium)

CBC with diffCBC with diff CulturesCultures PT/PTTPT/PTT LFTsLFTs

LactateLactate CortisolCortisol ThyroxineThyroxine Type and crossType and cross

Page 26: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Management of ShockManagement of Shock

Goal: Increase oxygen delivery & decrease Goal: Increase oxygen delivery & decrease oxygen demandoxygen demand

ABCsABCs Respiratory supportRespiratory support Fluid therapyFluid therapy Other therapiesOther therapies MonitoringMonitoring

Central venous pressure monitoringCentral venous pressure monitoring

Page 27: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Respiratory SupportRespiratory Support

Mechanical ventilation with adequate Mechanical ventilation with adequate sedation can decrease global oxygen sedation can decrease global oxygen demandsdemands

Early intubation:Early intubation: Improves oxygen deliveryImproves oxygen delivery Decreases afterload imposed by negative Decreases afterload imposed by negative

intrathoracic pressuresintrathoracic pressures Decreases burden of respiratory muscle fatigueDecreases burden of respiratory muscle fatigue

Page 28: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

IntubationIntubation

Use Ketamine Use Ketamine Pre-medicate with atropinePre-medicate with atropine Plan for ongoing sedationPlan for ongoing sedation

Do not use EtomidateDo not use Etomidate Associated with increased mortality in Associated with increased mortality in

adult and pediatric shockadult and pediatric shock

Page 29: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Fluid Therapy in ShockFluid Therapy in Shock

Goal is to optimize preload Goal is to optimize preload Isotonic fluids only (NS or LR)Isotonic fluids only (NS or LR)

20cc/kg aliquots q 2-10 minutes (except 20cc/kg aliquots q 2-10 minutes (except cardiogenic shock)cardiogenic shock)

Administer as fast as possibleAdminister as fast as possible At 60cc/kg reassess and if no responses At 60cc/kg reassess and if no responses

consider: ongoing losses, adrenal, consider: ongoing losses, adrenal, intestinal ischemia, obstructive shockintestinal ischemia, obstructive shock

CXRCXR Consider colloid Consider colloid

Page 30: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Fluid TherapyFluid Therapy

Follow heart rate, capillary perfusion, urine Follow heart rate, capillary perfusion, urine output, and blood pressureoutput, and blood pressure

Continue with fluid boluses until perfusion Continue with fluid boluses until perfusion and urine output restored, or pulmonary and urine output restored, or pulmonary congestion develops congestion develops

Hypovolemic shock responds dramatically Hypovolemic shock responds dramatically to fluid resuscitationto fluid resuscitation

Page 31: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Other therapies for ShockOther therapies for Shock

AntibioticsAntibiotics Correct acid base abnormalitiesCorrect acid base abnormalities Transfuse blood (increase oxygen carrying Transfuse blood (increase oxygen carrying

capacity)capacity) Prostaglandin if neonateProstaglandin if neonate Calcium if low ionized calciumCalcium if low ionized calcium Glucose for hypoglycemiaGlucose for hypoglycemia SedationSedation Vasoactive agentsVasoactive agents

Page 32: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Vasoactive AgentsVasoactive Agents

InotropesInotropes: effect myocardial : effect myocardial contractility and increase stroke contractility and increase stroke volumevolume

ChronotropesChronotropes: increase HR: increase HR PressorsPressors: increase SVR, usually : increase SVR, usually

increase blood pressureincrease blood pressure VasodilatorsVasodilators: reduce SVR/afterload : reduce SVR/afterload

Page 33: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

General classes of Vasoactive General classes of Vasoactive AgentsAgents

Alpha adrenergic (high dose epi and Alpha adrenergic (high dose epi and dopamine, norepi)dopamine, norepi)

Beta adrenergic (mid-dose dopamine, epi, Beta adrenergic (mid-dose dopamine, epi, dobutamine, isoproterenol)dobutamine, isoproterenol)

Dopaminergic (dopamine)Dopaminergic (dopamine) Vasodilators (venous, arterial, and pulmonaryVasodilators (venous, arterial, and pulmonary

—nitroglycerin, minoxidil, hydralyzine, —nitroglycerin, minoxidil, hydralyzine, nitroprusside, isoproterenol, inhaled NO)nitroprusside, isoproterenol, inhaled NO)

Other (milrinone, vasopressin, steroids)Other (milrinone, vasopressin, steroids)

Page 34: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Receptor TypesReceptor Types

Alpha adrenergicAlpha adrenergic alpha 1: vascular smooth muscle contraction alpha 1: vascular smooth muscle contraction

increases SVRincreases SVR alpha 2: vascular smooth muscle relaxation alpha 2: vascular smooth muscle relaxation

decreases SVR decreases SVR Beta adrenergic Beta adrenergic

beta 1: direct cardiac effects beta 1: direct cardiac effects increases SA node increases SA node rate, increased contractility, and coronary vasodilationrate, increased contractility, and coronary vasodilation

beta 2: smooth muscle relaxation beta 2: smooth muscle relaxation vasodilation and vasodilation and bronchodilationbronchodilation

Dopaminergic: Dopaminergic: Increases renal blood flow (low dose dopamine only)Increases renal blood flow (low dose dopamine only)

Page 35: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

DopamineDopamine

Both inotropic and vasopressor effectsBoth inotropic and vasopressor effects Use: treating shock with hypotension and Use: treating shock with hypotension and

decreased COdecreased CO Not good for hypovolemic shockNot good for hypovolemic shock Dose dependentDose dependent

Low dose selectively stimulates dopa receptors, Low dose selectively stimulates dopa receptors, vasodilation in renal, splanchnic, and cerebral vascular vasodilation in renal, splanchnic, and cerebral vascular beds beds

Mid dose are primary beta adrenergic effects (positive Mid dose are primary beta adrenergic effects (positive inotropy and chronotropy) to increase COinotropy and chronotropy) to increase CO

High dose are alpha adrenergic effects High dose are alpha adrenergic effects (vasoconstriction)(vasoconstriction)

Dose: start at 10 mcg/kg/min (mid-range dose)Dose: start at 10 mcg/kg/min (mid-range dose)

Page 36: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

DobutamineDobutamine

Mostly inotropic effects (increased SV and CO) Mostly inotropic effects (increased SV and CO) but with some vasoactive effect (peripheral but with some vasoactive effect (peripheral vasodilation). Acts directly on the Beta vasodilation). Acts directly on the Beta receptors.receptors.

Use: treating cardiogenic shock with myocardial Use: treating cardiogenic shock with myocardial dysfunction or inadequate cardiac output, dysfunction or inadequate cardiac output, patient with elevated SVR or PVRpatient with elevated SVR or PVR

Do not use in hypotensive patients until fluid Do not use in hypotensive patients until fluid resuscitatedresuscitated

Dose: start at 5 mcg/kg/minDose: start at 5 mcg/kg/min

Page 37: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

EpinephrineEpinephrine

Endogenous catecholamine that acts on alpha and Endogenous catecholamine that acts on alpha and beta adrenergic receptorsbeta adrenergic receptors

Use: inadequate cardiac output, hypotension, Use: inadequate cardiac output, hypotension, symptomatic bradycardia, pulseless cardiac arrest, symptomatic bradycardia, pulseless cardiac arrest, septic shock, cold shock septic shock, cold shock

Dose dependent Dose dependent Low dose: mostly beta effects (increased CO, mild Low dose: mostly beta effects (increased CO, mild

vasodilation)vasodilation) Mid dose: mixed beta 1 and alpha 1 effect (increased CO Mid dose: mixed beta 1 and alpha 1 effect (increased CO

with increased afterload)with increased afterload) High dose: mostly alpha 1 with increased SVR (can High dose: mostly alpha 1 with increased SVR (can

compromise renal and mesenteric blood flow)compromise renal and mesenteric blood flow) Dose: 0.1-1 mcg/kg/minDose: 0.1-1 mcg/kg/min

Page 38: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

NorepinephrineNorepinephrine

Similar to epinephrineSimilar to epinephrine Has alpha 1 and beta 1 effects but does Has alpha 1 and beta 1 effects but does

not cause beta 2 stimulation and has not cause beta 2 stimulation and has significant vasoconstrictor propertiessignificant vasoconstrictor properties

Use: shock with low SVR: warm shock, Use: shock with low SVR: warm shock, anaphylactic shock, spinal shockanaphylactic shock, spinal shock

Dose: 0.1-2 mcg/kg/minDose: 0.1-2 mcg/kg/min

Page 39: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

Other vasoactive agentsOther vasoactive agents

Phenylephrine: pure alpha effect, increase SVRPhenylephrine: pure alpha effect, increase SVR Isoproterenol: potent non-specific beta effectIsoproterenol: potent non-specific beta effect Milrinone: phosphodiesterase inhibitor, Milrinone: phosphodiesterase inhibitor,

increase inotropy, afterload reduction via increase inotropy, afterload reduction via vasodilationvasodilation

Nitroprusside: vasoactive agent, use with Nitroprusside: vasoactive agent, use with hypertension with low CO and high SVR hypertension with low CO and high SVR (monitor cyanide levels)(monitor cyanide levels)

Nitroglycerine: venodilating agent, coronary Nitroglycerine: venodilating agent, coronary arteries dilatorarteries dilator

Page 40: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital
Page 41: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

SummarySummary

Shock is a state of circulatory dysfunction that Shock is a state of circulatory dysfunction that leads to inadequate oxygen delivery or leads to inadequate oxygen delivery or utilization to meet the metabolic demands of utilization to meet the metabolic demands of cellscells

A high index of suspicion and early recognition A high index of suspicion and early recognition can prevent mortalitycan prevent mortality

Signs of symptoms of shock relate to poor skin Signs of symptoms of shock relate to poor skin perfusion and signs of end-organ perfusionperfusion and signs of end-organ perfusion

Early management of shock should occur Early management of shock should occur quickly: ABCs, fluid therapy to stabilize patient quickly: ABCs, fluid therapy to stabilize patient and then transfer to PICUand then transfer to PICU

Page 42: Shock Avni M. Bhalakia, M.D. St. Barnabas Hospital

ReferencesReferences

Bronicki, Ronald A. Shock States, Bronicki, Ronald A. Shock States, Pediatric Hospital Pediatric Hospital MedicineMedicine, 2003, 192-207., 2003, 192-207.

Clinical Practice Parameters for Hemodynamic support of Clinical Practice Parameters for Hemodynamic support of pediatric and neonatal septic shock: 2007 update from the pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine, American College of Critical Care Medicine, Critical Care Critical Care Medicine Medicine 2009, Vol 37, No 2, 666-688.2009, Vol 37, No 2, 666-688.

Davis, Alan L., Shock & Sepsis, downloaded from SCCM.org Davis, Alan L., Shock & Sepsis, downloaded from SCCM.org on september 1, 2009.on september 1, 2009.

Kiff, Jane E, Shock: Recognition and Treatment Strategies, Kiff, Jane E, Shock: Recognition and Treatment Strategies, Powerpoint handout given 2007.Powerpoint handout given 2007.

Pediatric Intensive Care Unit Handbook, Children’s National Pediatric Intensive Care Unit Handbook, Children’s National Medical Center, handout September 2004.Medical Center, handout September 2004.