1. SHOCK IN CHILDREN

2. Definition Circulatory system failure to supply
oxygen and nutrients to meet cellular
metabolic demands

3. Other Definitions Blood Pressure Cardiac Output Vascular Tone (SVR)
BP = CO x SVR
Cardiac Output
CO = SV X HR
Vascular Tone (SVR)
Regulated by several mechanisms

4. Oxygen Delivery DO2 = CO x CaO2 x 10
Remember: CO depends on HR, preload, afterload, and contractility
CaO2 = Hgb x 1.34 x SaO2 + (PaO2 x 0.003)
Remember: hemoglobin carries more than 99% of oxygen in the blood under standard conditions

5. Hemodynamics
Textbook of Pediatric Advanced Life Support, 1988

6. Defending the blood pressure
Neural Sympathetic
Baroreceptors
Carotid Body
Aortic Arch
Volume receptors
Right Atrium
Pulmonary vascular
Chemoreceptors
Aortic and carotid
Medullary
Cerebral ischemic response
Humoral
Adrenal medulla
Catecholamines
Hypothalamopituitary response
Adrenocorticotropic hormone
Vasopressin
Renin-angiotensin-aldosterone system

7. Cardiovascular function
Cardiac Output
Clinical Assessment
peripheral perfusion, temperature, capillary refill, urine output, mentation, acid-base status
CO = HR x SV
HR responds the quickest
SV is a function of three variables
preload, afterload, and myocardial contractility
A noncompliant heart cannot increase SV

8. Stroke Volume Preload (LVEDV) Reflects patient’s volume status
CVP or PCWP
Starling curve
Afterload
The resistance to ventricular ejection
Two variables:
vascular tone and transmural pressure
Myocardial Contractility (“squeeze”)
Many factors including coronary perfusion, baseline myocardial function, use of cardiotonic medications

9. Classification of Shock
COMPENSATED
blood flow is normal or increased and may be maldistributed; vital organ function is maintained
UNCOMPENSATED
microvascular perfusion is compromised; significant reductions in effective circulating volume
IRREVERSIBLE
inadequate perfusion of vital organs; irreparable damage; death cannot be prevented

10. Other Classifications
Hypovolemic or Hemorrhagic
Cardiogenic
Obstructive
Distributive

11. Cardiovascular Changes in Shock
Type Preload Afterload Contractility
Cardiogenic   
Hypovolemic   No change
Distributive   
Septic
early   
late   

12. Evaluation Regardless of the cause: ABC’s Respiratory Performance
First assess airway patency, ventilation, then circulatory system
Respiratory Performance
Respiratory rate and pattern, work of breathing, oxygenation (color), level of alertness
Circulation
Heart rate, BP, perfusion, and pulses, liver size
CVP monitoring may be helpful

13. Evaluation Early Signs of Shock sinus tachycardia
delayed capillary refill
fussy, irritable
Late Signs of Shock
bradycardia
altered mental status (lethargy, coma)
hypotonia, decreased DTR’s
Cheyne-Stokes breathing
hypotension is a very late sign
Lower limit of SBP = 70 + (2 x age in years)

14. Cardiovascular Assessment
Heart Rate
Too high: 180 bpm for infants, 160 bpm for children >1year old
Blood Pressure
Lower limit of SBP = (2 x age in years)
Peripheral Pulses
Present/Absent
Strength (diminished, normal, bounding)
Skin Perfusion
Capillary refill time
Temperature
Color
Mottling
CNS Perfusion
Recognition of parents
Reaction to pain
Muscle tone
Pupil size
Renal Perfusion
UOP >1cc/kg/hr

15. Treatment Airway management Always provide supplemental oxygen
Endotracheal intubation and controlled ventilation is suggested if respiratory failure or airway compromise is likely
elective is safer and less difficult
decrease negative intrathoracic pressure
improved oxygenation and O2 delivery and decreased O2 consumption
can hyperventilate if necessary

16. Treatment Circulation Based on presumed etiology
Rapid restoration of intravascular volume
PIV-if unstable you have seconds
I.O. if less than 4-6 years old
Central venous catheter
Use isotonic fluid: NS, LR, or 5% albumin
PRBC’s to replace blood loss or if still unstable after 60cc/kg of crystalloid
anemia is poorly tolerated in the stressed, hypoxic, hemodynamically unstable patient

17. Vasoactive/Cardiotonic Agents
Dopamine
1-5 mcg/kg/min: dopaminergic
5-15 mcg/kg/min: more beta-1
10-20 mcg/kg/min: more alpha-1
may be useful in distributive shock
Dobutamine
mcg/kg/min: mostly beta-1, some beta-2
may be useful in cardiogenic shock
Epinephrine
mcg/kg/min: mostly beta-1, some beta-2
> 0.1 to 0.2 mcg/kg/min: alpha-1

18. Vasoactive/Cardiotonic Agents
Norepinephrine
mcg/kg/min: only alpha and beta-1
Use up to 1mcg/kg/min
Milrinone
50mcg/kg load then mcg/kg/min: phosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effect on pulmonary vasculature)
Phenylephrine
mcg/kg/min: pure alpha

19. Hypovolemic # 1 cause of death in children worldwide Causes
Water Loss (diarrhea, vomiting with poor PO intake, diabetes, major burns)
Blood Loss (obvious trauma; occult bleeding from pelvic fractures, blunt abdominal trauma, “shaken baby”)
Low preload leads to decreased SV and decreased CO.
Compensation occurs with increased HR and SVR

20. Hypovolemic Shock Mainstay of therapy is fluid Goals
Restore intravascular volume
Correct metabolic acidosis
Treat the cause
Degree of dehydration often underestimated
Reassess perfusion, urine output, vital signs...
Isotonic crystalloid is always a good choice
20 to 50 cc/kg rapidly if cardiac function is normal
NS can cause a hyperchloremic acidosis

21. Treatment Solution Na+ Cl- K+ Ca++ Mg++ Buffer NS 154 154 0 0 0 None
LR Lactate
Plasmalyte Acetate & Gluconate
Inotropic and vasoactive drugs are not a substitute for fluid, however...
Can have various combinations of hypovolemic and septic and cardiogenic shock
May need to treat poor vascular tone and/or poor cardiac function

22. Hemorrhagic Shock Treatment is PRBCs or whole blood
Treat the cause if able (stop the bleeding)
Transfuse if significant blood loss is known or if patient unstable after 60cc/kg crystalloid
In an emergency can give group O PRBCs before cross matching is complete or type specific non-cross-matched blood products

23. Cardiogenic Low CO and high systemic vascular resistance
Result of primary cardiac dysfunction:
A compensatory increase in SVR occurs to maintain vital organ function
Subsequent increase in LV afterload, LV work, and cardiac oxygen consumption
CO decreases and ultimately results in volume retention, pulmonary edema, and RV failure

24. Cardiogenic Shock Etiologies
Congenital heart disease
Arrhythmias
Ischemic heart disease
Myocarditis
Myocardial injury
Acute and chronic drug toxicity
Late septic shock
Infiltrative diseases
mucopolysaccharidoses
glycogen storage diseases
Thyrotoxicosis
Pheochromocytoma

25. Cardiogenic Shock
Initial clinical presentation can be identical to hypovolemic shock
Initial therapy is a fluid challenge
If no improvement or if worsens after giving volume, suspect cardiogenic shock
Usually need invasive monitoring, further evaluation, pharmacologic therapy
Balancing fluid therapy and inotropic support can be very difficult.
Call an intensivist and/or a cardiologist

26. Obstructive Shock Low CO secondary to a physical obstruction to flow
Compensatory increased SVR
Causes:
Pericardial tamponade
Tension pneumothorax
Critical coarctation of the aorta
Aortic stenosis
Hypoplastic left heart syndrome

27. Obstructive Shock
Initial clinical presentation can be identical to hypovolemic shock
Initial therapy is a fluid challenge
Treat the cause
pericardial drain, chest tube, surgical intervention
if the patient is a neonate with a ductal dependent lesion then give PGE
Further evaluation, invasive monitoring, pharmacologic therapy, appropriate consults

28. Distributive Shock
High CO and low SVR (opposite of hypovolemic, cardiogenic, and obstructive)
Maldistribution of blood flow causing inadequate tissue perfusion
Due to release of endotoxin, vasoactive substances, complement cascade activation, and microcirculation thrombosis
Early septic shock is the most common form

29. Distributive Shock
Goal is to maintain intravascular volume and minimize increases in interstitial fluid (the primary problem is a decrease in SVR)
Use crystalloid initially
Additional fluid therapy should be based on lab studies
Can give up to 40cc/kg without monitoring CVP
Vasoactive/Cardiotonic agents often necessary
Treat the cause (i.e.. antimicrobial therapy)

30. Distributive Shock Etiologies
Anaphylaxis
Anaphylactoid reactions
Spinal cord injury/spinal shock
Head injury
Early sepsis
Drug intoxication
Barbiturates, Phenothiazines, Antihypertensives

31. Metabolic Issues Acid-Base
Metabolic acidosis develops secondary to tissue hypoperfusion
Profound acidosis depresses myocardial contractility and impairs the effectiveness of catecholamines
Tx: fluid administration and controlled ventilation
Buffer administration
Sodium Bicarbonate 1-2meq/kg or can calculate a 1/2 correction = 0.3 x weight (kg) x base deficit
hyperosmolarity, hypocalcemia, hypernatremia, left-ward shift of the oxyhemoglobin dissociation curve

32. Metabolic Issues Electrolytes
Calcium is important for cardiac function and for the pressor effect of catecholamines
Hypoglycemia can lead to CNS damage and is needed for proper cardiovascular function
Check the BUN and creatinine to evaluate renal function
Hyperkalemia can occur from renal dysfunction and/or acidosis

33. Metabolic Issues Special Topics
Congenital adrenal hyperplasia
Infant presents in shock, usually in the second week of life, typically a boy, with metabolic acidosis, hyponatremia, hypoglycemia, and hyperkalemia
Hyperammonemia
mild elevations are common with shock
levels > 1000 are consistent with inborn errors of metabolism
consider Reye Syndrome, toxins, hepatic failure

34. Other Studies Look for etiology of shock
Evaluate hemoglobin, hematocrit, and platelet count
Should be followed as these values may drop after fluid resuscitation
Shock from any etiology can lead to DIC and end organ damage
CBC, PT, INR, PTT, Fibrinogen, Factor V, Factor VIII, D-dimer, and/or FDPs
Check LFT’s, follow CNS and pulmonary status

35. Other Studies II Think about inborn errors of metabolism
Lactate and pyruvate
Ammonium, LFTs
Plasma amino acids, urine organic acids
Urinalysis with reducing substances
Urine tox screen

36. Conclusion
Goal of therapy is identification, evaluation, and treatment of shock in its earliest stage
Initial priorities are for the ABC’s
Fluid resuscitation begins with 20cc/kg of crystalloid or 10cc/kg of colloid
Subsequent treatment depends on the etiology of shock and the patient’s hemodynamic condition
Successful resuscitation depends on early and judicious intervention