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PEDIATRIC SHOCK. 2012. SHOCK. Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands Sequelae of shock are metabolic acidosis, organ dysfunction and death. SHOCK-OXGEN SUPPLY FAILS TO MEET OXYGEN DEMAND. OXYGEN SUPPLY. OXYGEN DEMAND. OYGEN DELIVERY.
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PEDIATRIC SHOCK 2012
SHOCK • Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands • Sequelae of shock are metabolic acidosis, organ dysfunction and death
SHOCK-OXGEN SUPPLY FAILS TO MEET OXYGEN DEMAND OXYGEN SUPPLY OXYGEN DEMAND
OYGEN DELIVERY CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT Cardiac Output Arterial oxygen content Hemoglobin Oxygen Saturation Partial pressure of oxygen dissolved in plasma Stroke Volume Heart rate Preload After load Contractility
Oxygen Delivery • Oxygen delivery=CO X Arterial oxygen content • CO=Heart rate X Stroke volume • Stroke volume depends on preload, afterload and contractility • Art Oxygen content= Hb x Sa02 x 1.34 +(0.003 x Pa02)
Factors affecting Oxygen delivery • Oxygenation-A-a gradient, DPG, acid base balance, Temp, Blockers • Stroke volume-Ventricular compliance, CVP, venous tone, autonomic tone, metabolic milieu, afterload, conduction system
Types of Shock • Hypovolemic- Hemorrhage, serum or plasma loss • Distributive-Anaphylactic, Neurogenic, septic • Cardiogenic- Myocardial, dysrrythmia, CHD(duct dependant) • Obstructive-Pneumo, tamponade, dissection • Dissociative-Heat, CO, cyanide, endocrine RJ has Hypovolemic shock secondary to Hemorrhage
Case 1 • 9 year old girl RJ with a history of variceal bleed presents with new onset bleed. O/E-responsive, HR-135, RR-38, BP-88/60, Sats-92%. I stat-7.08/24/80/12/-4. Hb-4.2 • What type of shock is this? Hypovolemic Shock • What is the very first thing you would like to do for this patient? Oxygen • Is this compensated or uncompensated shock- how does the body compensate? Compensated
Stages of Shock • Compensated- Vital organ function maintained, normal BP • Uncompensated-Marginal microvascular perfusion.Organ and cellular function deteriorate. Hypotension develops. • Irreversible RJ has compensated shock because her blood pressure is normal
Compensatory Mechanisms • Baroreceptors-In aortic arch and carotid sinus, low MAP cause vasoconstriction, increases BP, CO and HR • Chemoreceptors- Respond to cellular acidosis, results in vasoconstriction and respiratory stimulation
Compensatory Mechanisms • Renin Angiotensin- Decreased renal perfusion leads to angiotensin causing vasoconstriction and aldosterone causing salt and water retentions • Humoral Responses-Catecholamines • Autotransfusion-Reabsorption of interstitial fluid
RJ’s Clinical presentation • Diagnosis is based on exam focused on tissue perfusion • Neurological-Fluctuating mental status • Skin and extremities-Cool, pallor, mottling, cyanosis, poor cap refill, weak pulses, weak muscle tone • Cardio-pulmonary-Hyperpnea, tachycardia • Renal-Scant, concentrated urine • Abject hypotension is a late and premorbid sign( and is the flag for uncompensated shock)
Hypovolemic shock • Commonest cause worldwide • Decreased blood volume, decreased preload, decreased stroke volume • Signs of dehydration-tears, mucous membranes, skin tugor • Site of fluid loss may be obvious or concealed(liver, spleen, intracranial, GI)
Oxygen-What a difference! • Art Oxygen content= Hb x Sa02 x 1.34 +(0.003 x Pa02) • Pa02 on 100% is approx 650 • Pa02 on room air is approx 100 If your Hb is 15 this difference in PaO2 does not make much difference- if your Hb is 5 it makes all the difference!
RJ’s Management • Increase oxygen delivery, decrease oxygen demand • Oxygen • Fluid • Blood • Temperature control • Correct metabolic abnormalities • Inotrope if needed
Labs • ABG • Blood sugar • Electrolytes • CBC • PT/PTT/Fibrinogen • Type and Cross • Cultures • Imaging
Volume expansion • Optimize RJ’s preload with NS or RL • 10-20cc/kg q 2-10min. RJ is given 2 boluses. • RJ is given 2 units of blood. Her heart rate stabilizes at 86. BP-112/80. • RJ is deemed stable and gets sclerotherapy
Case 2 • TN is a 5 year old girl with a history of URI symptoms 2 weeks ago presents with decreased effort tolerance, tachypnea . O/E-HR-192, RR-70, BP-45 systolic. Hepatomegaly, b/l rales, no heart murmur on exam but a gallop is heard. • What type of shock is this? Uncompensated cardiogenic shock • What is the diagnosis? How do you manage this patient? Myocarditis
Differentiating Cardiogenic Shock • History • PE-enlarged liver, gallop, murmur, rales • Chest X ray-Enlarged heart, pulmonary venous congestion
OYGEN DELIVERY CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT Cardiac Output Arterial oxygen content Hemoglobin Oxygen Saturation Partial pressure of oxygen dissolved in plasma Stroke Volume Heart rate Preload After load Contractility
Managing TN • Increasing Oxygen supply- Supplemental Oxygen Improving myocardial output-altering preload, after load and contractility Correct Anemia-Blood • Decreasing oxygen demand- Control temperature Sedation Reduce myocardial work and thus oxygen consumption
Fluids in Cardiogenic Shock • Give small volume boluses of 5-10ml/kg • TN has myocarditis and because of this she has diastolic dysfunction- giving her extra fluid may overload her heart.
Ionotropes/Cardiotonics • Dopamine-Low dose increases renal and splanchnic blood flow, high dose increases HR and SVR. • Dobutamine- Increases contractility, may reduce SVR, PVR. • Milrinone-Inotropy and venodilation. Improve contractility and decrease after load
Ionotropes/ Cardiotonics • Epinephrine- Increases HR,SVR and contractility. End point-adequate BP, acceptable tachycardia • Norepinephrine-0.05-1.0mcg/kg/min. Increases SVR. Be hesitant to use either of these drugs for TN as they increase myocardial oxygen consumption
TN’s Hospital Course • 10ml/kg bolus with normal saline results in minimal elevation of blood pressure • Started on Dopamine of 5mcg/kg/min and Milrinone 0.5 mcg/kg/min • Stable for transport to Cardiac ICU • Attempted intubation results in circulatory collapse-TN goes up on ECMO
Other causes of Cardiogenic Shock • Dysrhythmia • Infection • Metabolic • Obstructive • Drugs • Congenital heart disease • Trauma
Case 3 • 4 year old boy RS presents with 3 day h/o fever, malaise. He has a past history of nephrotic syndrome.O/E-Minimally responsive,skin appears flushed and warm, and he has bounding pulses. HR-170 RR-30 BP-40 systolic, sats-88%. • What type of shock does the patient have Uncompensated distributive shock- Warm septic shock • What medications could be used in the management of this patient? Fluid, antibiotics, pressors, steroids
Septic Shock • Mediator release- both exogenous and endogenous lead to misdistribution of blood, imbalance of oxygen supply and demand, alterations in metabolism and cardiac dysfunction
Warm Shock • Early compensated hyperdynamic state of septic shock • Warm extremities, bounding pulses, tachycardia, wide pulse pressure, decreased systemic vascular resistance and increased cardiac output • Often with hyperglycemia
Cold Shock • Late uncompensated stage of septic shock with drop in cardiac output and increased SVR • Cold and clammy skin, rapid thready pulses, shallow breathing • Associated metabolic acidosis, hypoxia, coagulopathy, hypoglycemia, capillary leak
PALS ALGORITHM • 1ST hour-20ml/kg/boluses. • Correct hypoglycemia and hypocalcemia. • Administer 1st dose of antibiotics • Consider vasopressor drip and stress dose hydrocortisone • DETERMINE WHETHER FLUID RESPONSIVE
PALS ALGORITHM • IF NOT FLUID RESPONSIVE Normotensive-Start Dopamine Hypotensive vasodilated(warm shock)-Norepinephrine Hypotensive vasoconstricted(cold shock)-Epinephrine EVALUATE MIXED VENOUS SAT, GOAL>70%
RS- Hospital Course • 100ml/kg of fluid is given, BP improves to 60/30 • Started on Norepinephrine drip following which BP improves to systolic of 80. • Rt IJ placed ScVO2-74% • Hydrocortisone 2mg/kg-1 dose given • Starts Vancomycin and Ceftriaxone Microbiology calls to tell you there are Gram Neg rods on blood culture smear
PALS ALGORITHM • ScvO2>70%, Low BP, warm shock-Additional fluid. Norepinephrine +/- Vasopressin • ScvO2<70%, normal BP, poor perfusion-Transfuse to Hb>10g/dl. Consider milrinone/ nitroprusside/dobutamine • ScvO2<70%, low BP, poor perfusion-Transfuse to Hb>10g/dl. Consider epinephrine or dobutamine +norepinephrine • ADRENAL INSUFFICIENCY- Hydrocrtisone 2mg/kg
How much fluid is to much? • Fluids in early septic shock- Carcillo, JAMA 1991 • Three treatment groups 1-20cc/kg in first hour 2- Upto 40cc/kg in first hour 3- More than 40cc/kg in first hour NO DIFFERENCE IN ARDS BETWEEN GROUPS
Conclusions • Recognise shock quickly-tachycardia is the first sign, hypotension is late • Gain access quickly-if needed use IO. PIV better than a central line • If patient is not responding the way you think broaden your differential, think about other types of shock.