PEDIATRIC SHOCK by 45GhV20m

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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                                  OXYGEN
 SUPPLY                                  DEMAND
                           OYGEN DELIVERY




   CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT




      Cardiac                                Arterial oxygen content
      Output


                Stroke Volume        Hemoglobin
Heart rate
                                     Oxygen Saturation
                                     Partial pressure of oxygen dissolved in plasma

                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
RJ At Endoscopy
                      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
Myocarditis
                           OYGEN DELIVERY




   CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT




      Cardiac                                Arterial oxygen content
      Output


                Stroke Volume        Hemoglobin
Heart rate
                                     Oxygen Saturation
                                     Partial pressure of oxygen dissolved in plasma

                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.

								
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