1. PEDIATRIC SHOCK
2012

2. 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

3. SHOCK-OXGEN SUPPLY FAILS TO MEET OXYGEN DEMAND
OXYGEN SUPPLY
OXYGEN DEMAND

4. 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

5. 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 (0.003 x Pa02)

6. 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

7. 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

8. 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

9. 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

10. 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

11. 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

12. 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)

13. 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)

14. Oxygen-What a difference!
Art Oxygen content= Hb x Sa02 x (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!

15. RJ’s Management Increase oxygen delivery, decrease oxygen demand
Fluid
Blood
Temperature control
Correct metabolic abnormalities
Inotrope if needed

16. Labs ABG Blood sugar Electrolytes CBC PT/PTT/Fibrinogen Type and Cross
Cultures
Imaging

17. 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

18. RJ At Endoscopy

19. 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

20. Differentiating Cardiogenic Shock
History
PE-enlarged liver, gallop, murmur, rales
Chest X ray-Enlarged heart, pulmonary venous congestion

21. Myocarditis

22. 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

23. 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

24. 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.

25. 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

26. Ionotropes/ Cardiotonics
Epinephrine- Increases HR,SVR and contractility. End point-adequate BP, acceptable tachycardia
Norepinephrine mcg/kg/min. Increases SVR.
Be hesitant to use either of these drugs for TN as they increase myocardial oxygen consumption

27. 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

28. Other causes of Cardiogenic Shock
Dysrhythmia
Infection
Metabolic
Obstructive
Drugs
Congenital heart disease
Trauma

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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%

35. 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

36. 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

37. 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

38. 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.