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SHOCK IN CHILDRENSHOCK IN CHILDREN

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DefinitionDefinition

Circulatory system failure to supplyCirculatory system failure to supplyoxygen and nutrients to meet oxygen and nutrients to meet

cellularcellularmetabolic demandsmetabolic demands

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Other DefinitionsOther Definitions

• Blood PressureBlood PressureBP = CO x SVRBP = CO x SVR

• Cardiac OutputCardiac OutputCO = SV X HRCO = SV X HR

• Vascular Tone (SVR)Vascular Tone (SVR)– Regulated by several mechanismsRegulated by several mechanisms

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Oxygen DeliveryOxygen Delivery• DODO22 = CO x CaO = CO x CaO22 x 10 x 10

– Remember: CO depends on HR, preload, Remember: CO depends on HR, preload, afterload, and contractilityafterload, and contractility

• CaOCaO22 = Hgb x 1.34 x SaO = Hgb x 1.34 x SaO22 + (PaO + (PaO22 x 0.003) x 0.003) – Remember: hemoglobin carries more than Remember: hemoglobin carries more than

99% of oxygen in the blood under standard 99% of oxygen in the blood under standard conditions conditions

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HemodynamicsHemodynamicsMyocardialContractility

Stroke Volume Preload

Cardiac Output Afterload

Blood Pressure Heart Rate

Systemic Vascular Resistance

Textbook of Pediatric Advanced Life Support, 1988Textbook of Pediatric Advanced Life Support, 1988

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Defending the blood pressureDefending the blood pressure• Neural SympatheticNeural Sympathetic

– BaroreceptorsBaroreceptors• Carotid BodyCarotid Body• Aortic ArchAortic Arch

– Volume receptorsVolume receptors• Right AtriumRight Atrium• Pulmonary vascularPulmonary vascular

– ChemoreceptorsChemoreceptors• Aortic and carotidAortic and carotid• MedullaryMedullary

– Cerebral ischemic Cerebral ischemic responseresponse

• HumoralHumoral– Adrenal medullaAdrenal medulla

• CatecholaminesCatecholamines– HypothalamopituitarHypothalamopituitar

y responsey response• AdrenocorticotropiAdrenocorticotropi

c hormonec hormone• VasopressinVasopressin

– Renin-angiotensin-Renin-angiotensin-aldosterone systemaldosterone system

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Cardiovascular functionCardiovascular function

• Cardiac OutputCardiac Output Clinical AssessmentClinical Assessment

•peripheral perfusion, temperature, capillary peripheral perfusion, temperature, capillary refill, urine output, mentation, acid-base statusrefill, urine output, mentation, acid-base status

CO = HR x SVCO = HR x SV•HR responds the quickestHR responds the quickest•SV is a function of three variablesSV is a function of three variables– preload, afterload, and myocardial preload, afterload, and myocardial

contractilitycontractility•A noncompliant heart cannot increase SVA noncompliant heart cannot increase SV

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Stroke VolumeStroke Volume• Preload (LVEDV)Preload (LVEDV)

– Reflects patient’s volume statusReflects patient’s volume status– CVP or PCWPCVP or PCWP– Starling curveStarling curve

• AfterloadAfterload– The resistance to ventricular ejectionThe resistance to ventricular ejection– Two variables:Two variables:

• vascular tone and transmural pressurevascular tone and transmural pressure• Myocardial Contractility (“squeeze”)Myocardial Contractility (“squeeze”)

– Many factors including coronary perfusion, baseline Many factors including coronary perfusion, baseline myocardial function, use of cardiotonic medicationsmyocardial function, use of cardiotonic medications

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Classification of ShockClassification of Shock• COMPENSATEDCOMPENSATED

– blood flow is normal or increased and may be blood flow is normal or increased and may be maldistributed; vital organ function is maintainedmaldistributed; vital organ function is maintained

• UNCOMPENSATEDUNCOMPENSATED– microvascular perfusion is compromised; significant microvascular perfusion is compromised; significant

reductions in effective circulating volumereductions in effective circulating volume

• IRREVERSIBLEIRREVERSIBLE– inadequate perfusion of vital organs; irreparable inadequate perfusion of vital organs; irreparable

damage; death cannot be preventeddamage; death cannot be prevented

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Other ClassificationsOther Classifications• Hypovolemic or HemorrhagicHypovolemic or Hemorrhagic• CardiogenicCardiogenic• ObstructiveObstructive• DistributiveDistributive

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Cardiovascular Changes in ShockCardiovascular Changes in Shock

TypeType Preload Preload AfterloadAfterload ContractilityContractilityCardiogenic Cardiogenic Hypovolemic Hypovolemic No change No changeDistributive Distributive SepticSeptic

early early late late

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EvaluationEvaluation• Regardless of the cause: ABC’sRegardless of the cause: ABC’s

– First assess airway patency, ventilation, then First assess airway patency, ventilation, then circulatory systemcirculatory system

• Respiratory PerformanceRespiratory Performance– Respiratory rate and pattern, work of breathing, Respiratory rate and pattern, work of breathing,

oxygenation (color), level of alertnessoxygenation (color), level of alertness• CirculationCirculation

– Heart rate, BP, perfusion, and pulses, liver sizeHeart rate, BP, perfusion, and pulses, liver size– CVP monitoring may be helpfulCVP monitoring may be helpful

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EvaluationEvaluation• Early Signs of ShockEarly Signs of Shock

– sinus tachycardiasinus tachycardia– delayed capillary refilldelayed capillary refill– fussy, irritablefussy, irritable

• Late Signs of ShockLate Signs of Shock– bradycardiabradycardia– altered mental status (lethargy, coma)altered mental status (lethargy, coma)– hypotonia, decreased DTR’shypotonia, decreased DTR’s– Cheyne-Stokes breathingCheyne-Stokes breathing– hypotension is a very late sign hypotension is a very late sign – Lower limit of SBP = 70 + (2 x age in years)Lower limit of SBP = 70 + (2 x age in years)

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AssessmentAssessment• Heart RateHeart Rate

– Too high: 180 bpm for Too high: 180 bpm for infants, 160 bpm for infants, 160 bpm for children >1year oldchildren >1year old

• Blood PressureBlood Pressure– Lower limit of SBP = Lower limit of SBP =

70 + (2 x age in 70 + (2 x age in years)years)

• Peripheral PulsesPeripheral Pulses– Present/AbsentPresent/Absent– Strength (diminished, Strength (diminished,

normal, bounding)normal, bounding)

• Skin PerfusionSkin Perfusion– Capillary refill timeCapillary refill time– TemperatureTemperature– ColorColor– MottlingMottling

• CNS PerfusionCNS Perfusion– Recognition of parentsRecognition of parents– Reaction to painReaction to pain– Muscle toneMuscle tone– Pupil sizePupil size

• Renal PerfusionRenal Perfusion– UOP >1cc/kg/hrUOP >1cc/kg/hr

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TreatmentTreatmentAirway managementAirway management

– Always provide supplemental oxygenAlways provide supplemental oxygen– Endotracheal intubation and controlled Endotracheal intubation and controlled

ventilation is suggested if respiratory failure or ventilation is suggested if respiratory failure or airway compromise is likelyairway compromise is likely• elective is safer and less difficultelective is safer and less difficult•decrease negative intrathoracic pressure decrease negative intrathoracic pressure • improved oxygenation and Oimproved oxygenation and O22 delivery and delivery and

decreased Odecreased O22 consumption consumption• can hyperventilate if necessarycan hyperventilate if necessary

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TreatmentTreatmentCirculationCirculation

– Based on presumed etiology Based on presumed etiology – Rapid restoration of intravascular volumeRapid restoration of intravascular volume

•PIV-if unstable you have 60-90 secondsPIV-if unstable you have 60-90 seconds• I.O. if less than 4-6 years oldI.O. if less than 4-6 years old•Central venous catheterCentral venous catheter•Use isotonic fluid: NS, LR, or 5% albuminUse isotonic fluid: NS, LR, or 5% albumin•PRBC’s to replace blood loss or if still PRBC’s to replace blood loss or if still

unstable after 60cc/kg of crystalloid unstable after 60cc/kg of crystalloid – anemia is poorly tolerated in the stressed, anemia is poorly tolerated in the stressed,

hypoxic, hemodynamically unstable patienthypoxic, hemodynamically unstable patient

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AgentsAgents• DopamineDopamine

– 1-5 mcg/kg/min: dopaminergic1-5 mcg/kg/min: dopaminergic– 5-15 mcg/kg/min: more beta-15-15 mcg/kg/min: more beta-1– 10-20 mcg/kg/min: more alpha-110-20 mcg/kg/min: more alpha-1– may be useful in distributive shockmay be useful in distributive shock

• DobutamineDobutamine– 2.5-15 mcg/kg/min: mostly beta-1, some beta-22.5-15 mcg/kg/min: mostly beta-1, some beta-2– may be useful in cardiogenic shockmay be useful in cardiogenic shock

• EpinephrineEpinephrine– 0.05-0.1 mcg/kg/min: mostly beta-1, some beta-20.05-0.1 mcg/kg/min: mostly beta-1, some beta-2– > 0.1 to 0.2 mcg/kg/min: alpha-1> 0.1 to 0.2 mcg/kg/min: alpha-1

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AgentsAgents• NorepinephrineNorepinephrine

– 0.05-0.2mcg/kg/min: only alpha and beta-10.05-0.2mcg/kg/min: only alpha and beta-1– Use up to 1mcg/kg/minUse up to 1mcg/kg/min

• MilrinoneMilrinone– 50mcg/kg load then 0.375-0.75mcg/kg/min: 50mcg/kg load then 0.375-0.75mcg/kg/min:

phosphodiesterase inhibitor; results in increased phosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effect inotropy and peripheral vasodilation (greater effect on pulmonary vasculature)on pulmonary vasculature)

• PhenylephrinePhenylephrine– 0.1-0.5mcg/kg/min: pure alpha0.1-0.5mcg/kg/min: pure alpha

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HypovolemicHypovolemic• # 1 cause of death in children worldwide# 1 cause of death in children worldwide• CausesCauses

•Water Loss (diarrhea, vomiting with poor PO Water Loss (diarrhea, vomiting with poor PO intake, diabetes, major burns)intake, diabetes, major burns)

•Blood Loss (obvious trauma; occult bleeding Blood Loss (obvious trauma; occult bleeding from pelvic fractures, blunt abdominal from pelvic fractures, blunt abdominal trauma, “shaken baby”)trauma, “shaken baby”)

• Low preload leads to decreased SV and decreased Low preload leads to decreased SV and decreased CO.CO.

• Compensation occurs with increased HR and SVR Compensation occurs with increased HR and SVR

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Hypovolemic ShockHypovolemic Shock• Mainstay of therapy is Mainstay of therapy is fluidfluid• GoalsGoals

– Restore intravascular volumeRestore intravascular volume– Correct metabolic acidosisCorrect metabolic acidosis– Treat the causeTreat the cause

• Degree of dehydration often underestimatedDegree of dehydration often underestimated– Reassess perfusion, urine output, vital signs...Reassess perfusion, urine output, vital signs...

• Isotonic crystalloid is always a good choiceIsotonic crystalloid is always a good choice– 20 to 50 cc/kg rapidly if cardiac function is 20 to 50 cc/kg rapidly if cardiac function is

normalnormal– NS can cause a hyperchloremic acidosisNS can cause a hyperchloremic acidosis

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TreatmentTreatmentSolution Na+ Cl- K+ Ca++ Mg++ BufferSolution Na+ Cl- K+ Ca++ Mg++ BufferNS 154 154 0 0 0 NoneNS 154 154 0 0 0 NoneLR 130 109 4 3 0 Lactate LR 130 109 4 3 0 Lactate Plasmalyte 140 98 5 0 3 Acetate Plasmalyte 140 98 5 0 3 Acetate

& Gluconate & Gluconate

Inotropic and vasoactive drugs are not a substitute for fluid, Inotropic and vasoactive drugs are not a substitute for fluid, however...however...– Can have various combinations of hypovolemic and septic Can have various combinations of hypovolemic and septic

and cardiogenic shockand cardiogenic shock– May need to treat poor vascular tone and/or poor cardiac May need to treat poor vascular tone and/or poor cardiac

functionfunction

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Hemorrhagic ShockHemorrhagic Shock• Treatment is PRBCs or whole bloodTreatment is PRBCs or whole blood

– Treat the cause if able (stop the bleeding)Treat the cause if able (stop the bleeding)– Transfuse if significant blood loss is Transfuse if significant blood loss is

known or if patient unstable after 60cc/kg known or if patient unstable after 60cc/kg crystalloidcrystalloid• In an emergency can give group O In an emergency can give group O

PRBCs before cross matching is PRBCs before cross matching is complete or type specific non-cross-complete or type specific non-cross-matched blood productsmatched blood products

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CardiogenicCardiogenic• Low CO and high systemic vascular Low CO and high systemic vascular

resistanceresistance• Result of primary cardiac dysfunction:Result of primary cardiac dysfunction:

A compensatory increase in SVR occurs A compensatory increase in SVR occurs to maintain vital organ functionto maintain vital organ function

Subsequent increase in LV afterload, LV Subsequent increase in LV afterload, LV work, and cardiac oxygen consumptionwork, and cardiac oxygen consumption

CO decreases and ultimately results in CO decreases and ultimately results in volume retention, pulmonary edema, volume retention, pulmonary edema, and RV failureand RV failure

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Cardiogenic ShockCardiogenic ShockEtiologiesEtiologies• Congenital heart Congenital heart

diseasedisease• ArrhythmiasArrhythmias• Ischemic heart Ischemic heart

diseasedisease• MyocarditisMyocarditis• Myocardial injuryMyocardial injury• Acute and chronic Acute and chronic

drug toxicitydrug toxicity

• Late septic shockLate septic shock• Infiltrative diseasesInfiltrative diseases

– mucopolysaccharidosemucopolysaccharidosess

– glycogen storage glycogen storage diseasesdiseases

• ThyrotoxicosisThyrotoxicosis• PheochromocytomaPheochromocytoma

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Cardiogenic ShockCardiogenic Shock• Initial clinical presentation can be identical to Initial clinical presentation can be identical to

hypovolemic shockhypovolemic shock• Initial therapy is a fluid challengeInitial therapy is a fluid challenge• If no improvement or if worsens after giving If no improvement or if worsens after giving

volume, suspect cardiogenic shockvolume, suspect cardiogenic shock• Usually need invasive monitoring, further Usually need invasive monitoring, further

evaluation, pharmacologic therapyevaluation, pharmacologic therapy• Balancing fluid therapy and inotropic support Balancing fluid therapy and inotropic support

can be very difficult. can be very difficult. – Call an intensivist and/or a cardiologistCall an intensivist and/or a cardiologist

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Obstructive ShockObstructive Shock• Low CO secondary to a physical obstruction to Low CO secondary to a physical obstruction to

flowflow• Compensatory increased SVRCompensatory increased SVR• Causes:Causes:

– Pericardial tamponade Pericardial tamponade – Tension pneumothorax Tension pneumothorax – Critical coarctation of the aorta Critical coarctation of the aorta – Aortic stenosis Aortic stenosis – Hypoplastic left heart syndromeHypoplastic left heart syndrome

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Obstructive ShockObstructive Shock• Initial clinical presentation can be identical to Initial clinical presentation can be identical to

hypovolemic shockhypovolemic shock• Initial therapy is a fluid challengeInitial therapy is a fluid challenge• Treat the causeTreat the cause

– pericardial drain, chest tube, surgical pericardial drain, chest tube, surgical interventionintervention

– if the patient is a neonate with a ductal if the patient is a neonate with a ductal dependent lesion then give PGEdependent lesion then give PGE

• Further evaluation, invasive monitoring, Further evaluation, invasive monitoring, pharmacologic therapy, appropriate consultspharmacologic therapy, appropriate consults

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Distributive ShockDistributive Shock• High CO and low SVR (opposite of High CO and low SVR (opposite of

hypovolemic, cardiogenic, and obstructive)hypovolemic, cardiogenic, and obstructive)• Maldistribution of blood flow causing Maldistribution of blood flow causing

inadequate tissue perfusioninadequate tissue perfusion• Due to release of endotoxin, vasoactive Due to release of endotoxin, vasoactive

substances, complement cascade substances, complement cascade activation, and microcirculation thrombosisactivation, and microcirculation thrombosis

• Early septic shock is the most common formEarly septic shock is the most common form

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Distributive ShockDistributive Shock• Goal is to maintain intravascular volume and Goal is to maintain intravascular volume and

minimize increases in interstitial fluid (the minimize increases in interstitial fluid (the primary problem is a decrease in SVR)primary problem is a decrease in SVR)– Use crystalloid initiallyUse crystalloid initially– Additional fluid therapy should be based on lab Additional fluid therapy should be based on lab

studiesstudies– Can give up to 40cc/kg without monitoring CVPCan give up to 40cc/kg without monitoring CVP– Vasoactive/Cardiotonic agents often necessaryVasoactive/Cardiotonic agents often necessary– Treat the cause (i.e.. antimicrobial therapy)Treat the cause (i.e.. antimicrobial therapy)

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Distributive ShockDistributive ShockEtiologiesEtiologies• AnaphylaxisAnaphylaxis• Anaphylactoid reactionsAnaphylactoid reactions• Spinal cord injury/spinal shockSpinal cord injury/spinal shock• Head injuryHead injury• Early sepsisEarly sepsis• Drug intoxicationDrug intoxication

– Barbiturates, Phenothiazines, Barbiturates, Phenothiazines, AntihypertensivesAntihypertensives

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Metabolic IssuesMetabolic IssuesAcid-BaseAcid-Base• Metabolic acidosis develops secondary to tissue Metabolic acidosis develops secondary to tissue

hypoperfusionhypoperfusion• Profound acidosis depresses myocardial Profound acidosis depresses myocardial

contractility and impairs the effectiveness of contractility and impairs the effectiveness of catecholaminescatecholamines

• Tx: fluid administration and controlled ventilationTx: fluid administration and controlled ventilation• Buffer administrationBuffer administration

– Sodium Bicarbonate 1-2meq/kg or can calculate a 1/2 Sodium Bicarbonate 1-2meq/kg or can calculate a 1/2 correction = 0.3 x weight (kg) x base deficitcorrection = 0.3 x weight (kg) x base deficit

– hyperosmolarity, hypocalcemia, hypernatremia, left-hyperosmolarity, hypocalcemia, hypernatremia, left-ward shift of the oxyhemoglobin dissociation curveward shift of the oxyhemoglobin dissociation curve

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Metabolic IssuesMetabolic IssuesElectrolytesElectrolytes• ElectrolytesElectrolytes

– Calcium is important for cardiac function and Calcium is important for cardiac function and for the pressor effect of catecholaminesfor the pressor effect of catecholamines

– Hypoglycemia can lead to CNS damage and Hypoglycemia can lead to CNS damage and is needed for proper cardiovascular functionis needed for proper cardiovascular function

– Check the BUN and creatinine to evaluate Check the BUN and creatinine to evaluate renal functionrenal function

– Hyperkalemia can occur from renal Hyperkalemia can occur from renal dysfunction and/or acidosisdysfunction and/or acidosis

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Metabolic IssuesMetabolic IssuesSpecial TopicsSpecial TopicsCongenital adrenal hyperplasiaCongenital adrenal hyperplasia

• Infant presents in shock, usually in the second Infant presents in shock, usually in the second week of life, typically a boy, with metabolic week of life, typically a boy, with metabolic acidosis, hyponatremia, hypoglycemia, and acidosis, hyponatremia, hypoglycemia, and hyperkalemiahyperkalemia

HyperammonemiaHyperammonemia•mild elevations are common with shockmild elevations are common with shock• levels > 1000 are consistent with inborn errors levels > 1000 are consistent with inborn errors

of metabolism of metabolism • consider Reye Syndrome, toxins, hepatic failureconsider Reye Syndrome, toxins, hepatic failure

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Other StudiesOther Studies• Look for etiology of shockLook for etiology of shock• Evaluate hemoglobin, hematocrit, and Evaluate hemoglobin, hematocrit, and

platelet countplatelet count– Should be followed as these values may drop Should be followed as these values may drop

after fluid resuscitationafter fluid resuscitation• Shock from any etiology can lead to DIC and Shock from any etiology can lead to DIC and

end organ damageend organ damage– CBC, PT, INR, PTT, Fibrinogen, Factor V, CBC, PT, INR, PTT, Fibrinogen, Factor V,

Factor VIII, D-dimer, and/or FDPsFactor VIII, D-dimer, and/or FDPs– Check LFT’s, follow CNS and pulmonary statusCheck LFT’s, follow CNS and pulmonary status

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Other Studies IIOther Studies II

• Think about inborn errors of metabolismThink about inborn errors of metabolism– Lactate and pyruvateLactate and pyruvate– Ammonium, LFTsAmmonium, LFTs– Plasma amino acids, urine organic acidsPlasma amino acids, urine organic acids– Urinalysis with reducing substancesUrinalysis with reducing substances– Urine tox screenUrine tox screen

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ConclusionConclusion• Goal of therapy is identification, evaluation, Goal of therapy is identification, evaluation,

and treatment of shock in its earliest stageand treatment of shock in its earliest stage• Initial priorities are for the ABC’sInitial priorities are for the ABC’s• Fluid resuscitation begins with 20cc/kg of Fluid resuscitation begins with 20cc/kg of

crystalloid or 10cc/kg of colloidcrystalloid or 10cc/kg of colloid• Subsequent treatment depends on the etiology Subsequent treatment depends on the etiology

of shock and the patient’s hemodynamic of shock and the patient’s hemodynamic conditioncondition

• Successful resuscitation depends on early and Successful resuscitation depends on early and judicious interventionjudicious intervention