PEDIATRIC PEDIATRIC SHOCKSHOCK

20122012

SHOCKSHOCK

Shock is a syndrome that results Shock is a syndrome that results from inadequate oxygen delivery to from inadequate oxygen delivery to meet metabolic demandsmeet metabolic demands

Sequelae of shock are metabolic Sequelae of shock are metabolic acidosis, organ dysfunction and acidosis, organ dysfunction and deathdeath

OXYGEN SUPPLY

OXYGEN DEMAND

SHOCK-OXGEN SUPPLY FAILS TO MEET OXYGEN DEMAND

OYGEN DELIVERY

CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT

Cardiac Output

Arterial oxygen content

Heart rate Stroke Volume

PreloadAfter loadContractility

HemoglobinOxygen SaturationPartial pressure of oxygen dissolved in plasma

Oxygen DeliveryOxygen Delivery

Oxygen delivery=CO X Arterial Oxygen delivery=CO X Arterial oxygen contentoxygen content

CO=Heart rate X Stroke volumeCO=Heart rate X Stroke volume Stroke volume depends on preload, Stroke volume depends on preload,

afterload and contractilityafterload and contractility Art Oxygen content= Hb x Sa02 x Art Oxygen content= Hb x Sa02 x

1.34 +(0.003 x Pa02)1.34 +(0.003 x Pa02)

Factors affecting Oxygen Factors affecting Oxygen deliverydelivery

Oxygenation-A-a gradient, DPG, acid Oxygenation-A-a gradient, DPG, acid base balance, Temp, Blockersbase balance, Temp, Blockers

Stroke volume-Ventricular Stroke volume-Ventricular compliance, CVP, venous tone, compliance, CVP, venous tone, autonomic tone, metabolic milieu, autonomic tone, metabolic milieu, afterload, conduction systemafterload, conduction system

Types of ShockTypes of Shock Hypovolemic- Hemorrhage, serum or Hypovolemic- Hemorrhage, serum or

plasma lossplasma loss Distributive-Anaphylactic, Neurogenic, Distributive-Anaphylactic, Neurogenic,

septicseptic Cardiogenic- Myocardial, dysrrythmia, Cardiogenic- Myocardial, dysrrythmia,

CHD(duct dependant)CHD(duct dependant) Obstructive-Pneumo, tamponade, dissectionObstructive-Pneumo, tamponade, dissection Dissociative-Heat, CO, cyanide, endocrineDissociative-Heat, CO, cyanide, endocrine

RJ has Hypovolemic shock secondary to RJ has Hypovolemic shock secondary to HemorrhageHemorrhage

Case 1Case 1 9 year old girl RJ with a history of variceal bleed 9 year old girl RJ with a history of variceal bleed

presents with new onset bleed. O/E-responsive, presents with new onset bleed. O/E-responsive, HR-135, RR-38, BP-88/60, Sats-92%. I stat-HR-135, RR-38, BP-88/60, Sats-92%. I stat-7.08/24/80/12/-4. Hb-4.27.08/24/80/12/-4. Hb-4.2

What type of shock is this? What type of shock is this? Hypovolemic ShockHypovolemic Shock What is the very first thing you would like to do What is the very first thing you would like to do

for this patient?for this patient?OxygenOxygen Is this compensated or uncompensated shock- Is this compensated or uncompensated shock-

how does the body compensate?how does the body compensate?CompensatedCompensated

Stages of ShockStages of Shock

Compensated- Vital organ function Compensated- Vital organ function maintained, normal BPmaintained, normal BP

Uncompensated-Marginal Uncompensated-Marginal microvascular perfusion.Organ and microvascular perfusion.Organ and cellular function deteriorate. cellular function deteriorate. Hypotension develops.Hypotension develops.

IrreversibleIrreversible

RJ has compensated shock because her RJ has compensated shock because her blood pressure is normalblood pressure is normal

Compensatory Compensatory MechanismsMechanisms

Baroreceptors-In aortic arch and Baroreceptors-In aortic arch and carotid sinus, low MAP cause carotid sinus, low MAP cause vasoconstriction, increases BP, CO vasoconstriction, increases BP, CO and HRand HR

Chemoreceptors- Respond to cellular Chemoreceptors- Respond to cellular acidosis, results in vasoconstriction acidosis, results in vasoconstriction and respiratory stimulationand respiratory stimulation

Compensatory Compensatory MechanismsMechanisms

Renin Angiotensin- Decreased renal Renin Angiotensin- Decreased renal perfusion leads to angiotensin perfusion leads to angiotensin causing vasoconstriction and causing vasoconstriction and aldosterone causing salt and water aldosterone causing salt and water retentionsretentions

Humoral Responses-CatecholaminesHumoral Responses-Catecholamines Autotransfusion-Reabsorption of Autotransfusion-Reabsorption of

interstitial fluidinterstitial fluid

RJ’s Clinical presentationRJ’s Clinical presentation Diagnosis is based on exam focused on tissue Diagnosis is based on exam focused on tissue

perfusionperfusion Neurological-Fluctuating mental statusNeurological-Fluctuating mental status Skin and extremities-Cool, pallor, mottling, Skin and extremities-Cool, pallor, mottling,

cyanosis, poor cap refill, weak pulses, weak cyanosis, poor cap refill, weak pulses, weak muscle tonemuscle tone

Cardio-pulmonary-Hyperpnea, tachycardiaCardio-pulmonary-Hyperpnea, tachycardia Renal-Scant, concentrated urineRenal-Scant, concentrated urine

Abject hypotension is a late and premorbid Abject hypotension is a late and premorbid sign( and is the flag for uncompensated shock)sign( and is the flag for uncompensated shock)

Hypovolemic shockHypovolemic shock

Commonest cause worldwideCommonest cause worldwide Decreased blood volume, decreased Decreased blood volume, decreased

preload, decreased stroke volumepreload, decreased stroke volume Signs of dehydration-tears, mucous Signs of dehydration-tears, mucous

membranes, skin tugormembranes, skin tugor Site of fluid loss may be obvious or Site of fluid loss may be obvious or

concealed(liver, spleen, intracranial, concealed(liver, spleen, intracranial, GI)GI)

Oxygen-What a Oxygen-What a difference!difference!

Art Oxygen content= Hb x Sa02 x Art Oxygen content= Hb x Sa02 x 1.34 +(0.003 x Pa02)1.34 +(0.003 x Pa02)

Pa02 on 100% is approx 650Pa02 on 100% is approx 650 Pa02 on room air is approx 100Pa02 on room air is approx 100

If your Hb is 15 this difference in If your Hb is 15 this difference in PaO2 does not make much difference- PaO2 does not make much difference- if your Hb is 5 it makes all the if your Hb is 5 it makes all the difference!difference!

RJ’s ManagementRJ’s Management

Increase oxygen delivery, decrease Increase oxygen delivery, decrease oxygen demandoxygen demand

OxygenOxygen FluidFluid BloodBlood Temperature controlTemperature control Correct metabolic abnormalitiesCorrect metabolic abnormalities Inotrope if neededInotrope if needed

LabsLabs

ABGABG Blood sugarBlood sugar ElectrolytesElectrolytes CBCCBC PT/PTT/FibrinogenPT/PTT/Fibrinogen Type and CrossType and Cross CulturesCultures ImagingImaging

Volume expansionVolume expansion

Optimize RJ’s preload with NS or RLOptimize RJ’s preload with NS or RL 10-20cc/kg q 2-10min. RJ is given 2 10-20cc/kg q 2-10min. RJ is given 2

boluses.boluses. RJ is given 2 units of blood. Her RJ is given 2 units of blood. Her

heart rate stabilizes at 86. BP-heart rate stabilizes at 86. BP-112/80.112/80.

RJ is deemed stable and gets RJ is deemed stable and gets sclerotherapysclerotherapy

RJ At EndoscopyRJ At Endoscopy

Case 2Case 2 TN is a 5 year old girl with a history of TN is a 5 year old girl with a history of

URI symptoms 2 weeks ago presents with URI symptoms 2 weeks ago presents with decreased effort tolerance, tachypnea . decreased effort tolerance, tachypnea . O/E-HR-192, RR-70, BP-45 systolic. O/E-HR-192, RR-70, BP-45 systolic. Hepatomegaly, b/l rales, no heart murmur Hepatomegaly, b/l rales, no heart murmur on exam but a gallop is heard.on exam but a gallop is heard.

What type of shock is this?What type of shock is this?Uncompensated cardiogenic shockUncompensated cardiogenic shock What is the diagnosis? How do you What is the diagnosis? How do you

manage this patient?manage this patient?MyocarditisMyocarditis

Differentiating Cardiogenic Differentiating Cardiogenic ShockShock

HistoryHistory PE-enlarged liver, gallop, murmur, PE-enlarged liver, gallop, murmur,

ralesrales Chest X ray-Enlarged heart, Chest X ray-Enlarged heart,

pulmonary venous congestionpulmonary venous congestion

MyocarditisMyocarditis

OYGEN DELIVERY

CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT

Cardiac Output

Arterial oxygen content

Heart rate Stroke Volume

PreloadAfter loadContractility

HemoglobinOxygen SaturationPartial pressure of oxygen dissolved in plasma

Managing TNManaging TN Increasing Oxygen supply-Increasing Oxygen supply-Supplemental OxygenSupplemental OxygenImproving myocardial output-altering Improving myocardial output-altering

preload, after load and contractilitypreload, after load and contractilityCorrect Anemia-BloodCorrect Anemia-Blood Decreasing oxygen demand-Decreasing oxygen demand-Control temperatureControl temperatureSedationSedationReduce myocardial work and thus oxygen Reduce myocardial work and thus oxygen

consumptionconsumption

Fluids in Cardiogenic Fluids in Cardiogenic ShockShock

Give small volume boluses of 5-Give small volume boluses of 5-10ml/kg10ml/kg

TN has myocarditis and because of TN has myocarditis and because of this she has diastolic dysfunction- this she has diastolic dysfunction- giving her extra fluid may overload giving her extra fluid may overload her heart.her heart.

Ionotropes/CardiotonicsIonotropes/Cardiotonics

Dopamine-Low dose increases renal and Dopamine-Low dose increases renal and splanchnic blood flow, high dose increases splanchnic blood flow, high dose increases HR and SVR. HR and SVR.

Dobutamine- Increases contractility, may Dobutamine- Increases contractility, may reduce SVR, PVR. reduce SVR, PVR.

Milrinone-Inotropy and venodilation. Milrinone-Inotropy and venodilation. Improve contractility and decrease after Improve contractility and decrease after loadload

Ionotropes/ CardiotonicsIonotropes/ Cardiotonics

Epinephrine- Increases HR,SVR and Epinephrine- Increases HR,SVR and contractility. End point-adequate BP, contractility. End point-adequate BP, acceptable tachycardiaacceptable tachycardia

Norepinephrine-0.05-1.0mcg/kg/min. Increases Norepinephrine-0.05-1.0mcg/kg/min. Increases SVR. SVR.

Be hesitant to use either of these drugs for TN as Be hesitant to use either of these drugs for TN as they increase myocardial oxygen consumptionthey increase myocardial oxygen consumption

TN’s Hospital CourseTN’s Hospital Course

10ml/kg bolus with normal saline 10ml/kg bolus with normal saline results in minimal elevation of blood results in minimal elevation of blood pressurepressure

Started on Dopamine of 5mcg/kg/min Started on Dopamine of 5mcg/kg/min and Milrinone 0.5 mcg/kg/minand Milrinone 0.5 mcg/kg/min

Stable for transport to Cardiac ICUStable for transport to Cardiac ICU Attempted intubation results in Attempted intubation results in

circulatory collapse-TN goes up on circulatory collapse-TN goes up on ECMOECMO

Other causes of Other causes of Cardiogenic ShockCardiogenic Shock

DysrhythmiaDysrhythmia InfectionInfection MetabolicMetabolic ObstructiveObstructive DrugsDrugs Congenital heart diseaseCongenital heart disease TraumaTrauma

Case 3Case 3 4 year old boy RS presents with 3 day h/o fever, 4 year old boy RS presents with 3 day h/o fever,

malaise. He has a past history of nephrotic malaise. He has a past history of nephrotic syndrome.O/E-Minimally responsive,skin appears syndrome.O/E-Minimally responsive,skin appears flushed and warm, and he has bounding pulses. HR-flushed and warm, and he has bounding pulses. HR-170 RR-30 BP-40 systolic, sats-88%. 170 RR-30 BP-40 systolic, sats-88%.

What type of shock does the patient haveWhat type of shock does the patient haveUncompensated distributive shock- Warm septic shockUncompensated distributive shock- Warm septic shock What medications could be used in the management What medications could be used in the management

of this patient?of this patient?Fluid, antibiotics, pressors, steroidsFluid, antibiotics, pressors, steroids

Septic ShockSeptic Shock

Mediator release- both exogenous Mediator release- both exogenous and endogenous lead to and endogenous lead to misdistribution of blood, imbalance misdistribution of blood, imbalance of oxygen supply and demand, of oxygen supply and demand, alterations in metabolism and alterations in metabolism and cardiac dysfunctioncardiac dysfunction

Warm ShockWarm Shock

Early compensated hyperdynamic Early compensated hyperdynamic state of septic shockstate of septic shock

Warm extremities, bounding pulses, Warm extremities, bounding pulses, tachycardia, wide pulse pressure, tachycardia, wide pulse pressure, decreased systemic vascular decreased systemic vascular resistance and increased cardiac resistance and increased cardiac outputoutput

Often with hyperglycemiaOften with hyperglycemia

Cold ShockCold Shock

Late uncompensated stage of septic Late uncompensated stage of septic shock with drop in cardiac output shock with drop in cardiac output and increased SVRand increased SVR

Cold and clammy skin, rapid thready Cold and clammy skin, rapid thready pulses, shallow breathingpulses, shallow breathing

Associated metabolic acidosis, Associated metabolic acidosis, hypoxia, coagulopathy, hypoxia, coagulopathy, hypoglycemia, capillary leakhypoglycemia, capillary leak

PALS ALGORITHMPALS ALGORITHM

11STST hour-20ml/kg/boluses. hour-20ml/kg/boluses. Correct hypoglycemia and Correct hypoglycemia and

hypocalcemia. hypocalcemia. Administer 1Administer 1stst dose of antibiotics dose of antibiotics Consider vasopressor drip and stress Consider vasopressor drip and stress

dose hydrocortisonedose hydrocortisone DETERMINE WHETHER FLUID DETERMINE WHETHER FLUID

RESPONSIVE RESPONSIVE

PALS ALGORITHMPALS ALGORITHM

IF NOT FLUID RESPONSIVEIF NOT FLUID RESPONSIVE

Normotensive-Start DopamineNormotensive-Start Dopamine

Hypotensive vasodilated(warm shock)-Hypotensive vasodilated(warm shock)-NorepinephrineNorepinephrine

Hypotensive vasoconstricted(cold Hypotensive vasoconstricted(cold shock)-Epinephrineshock)-Epinephrine

EVALUATE MIXED VENOUS SAT, EVALUATE MIXED VENOUS SAT, GOAL>70%GOAL>70%

RS- Hospital CourseRS- Hospital Course

100ml/kg of fluid is given, BP improves to 100ml/kg of fluid is given, BP improves to 60/3060/30

Started on Norepinephrine drip following Started on Norepinephrine drip following which BP improves to systolic of 80.which BP improves to systolic of 80.

Rt IJ placed ScVO2-74%Rt IJ placed ScVO2-74% Hydrocortisone 2mg/kg-1 dose givenHydrocortisone 2mg/kg-1 dose given Starts Vancomycin and CeftriaxoneStarts Vancomycin and Ceftriaxone

Microbiology calls to tell you there are Gram Microbiology calls to tell you there are Gram Neg rods on blood culture smearNeg rods on blood culture smear

PALS ALGORITHMPALS ALGORITHM ScvO2>70%, Low BP, warm shock-Additional ScvO2>70%, Low BP, warm shock-Additional

fluid. Norepinephrine +/- Vasopressinfluid. Norepinephrine +/- Vasopressin ScvO2<70%, normal BP, poor perfusion-ScvO2<70%, normal BP, poor perfusion-

Transfuse to Hb>10g/dl. Consider milrinone/ Transfuse to Hb>10g/dl. Consider milrinone/ nitroprusside/dobutaminenitroprusside/dobutamine

ScvO2<70%, low BP, poor perfusion-ScvO2<70%, low BP, poor perfusion-Transfuse to Hb>10g/dl. Consider Transfuse to Hb>10g/dl. Consider epinephrine or dobutamine +norepinephrineepinephrine or dobutamine +norepinephrine

ADRENAL INSUFFICIENCY-ADRENAL INSUFFICIENCY- Hydrocrtisone 2mg/kgHydrocrtisone 2mg/kg

How much fluid is to How much fluid is to much?much?

Fluids in early septic shock- Carcillo, Fluids in early septic shock- Carcillo, JAMA 1991JAMA 1991

Three treatment groupsThree treatment groups1-20cc/kg in first hour1-20cc/kg in first hour2- Upto 40cc/kg in first hour2- Upto 40cc/kg in first hour3- More than 40cc/kg in first hour3- More than 40cc/kg in first hourNO DIFFERENCE IN ARDS NO DIFFERENCE IN ARDS

BETWEEN GROUPSBETWEEN GROUPS

ConclusionsConclusions

Recognise shock quickly-tachycardia Recognise shock quickly-tachycardia is the first sign, hypotension is lateis the first sign, hypotension is late

Gain access quickly-if needed use Gain access quickly-if needed use IO. PIV better than a central lineIO. PIV better than a central line

If patient is not responding the way If patient is not responding the way you think broaden your differential, you think broaden your differential, think about other types of shock.think about other types of shock.