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.
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