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SHOCK IN CHILDREN
Definition
Circulatory system failure to supply oxygen and nutrients to meet cellular metabolic demands
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Other Definitions
Blood Pressure
BP = CO x SVR
Cardiac Output
CO = SV X HR
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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
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Hemodynamics
Myocardial Contractility Stroke Volume Cardiac Output Blood Pressure Systemic Vascular Resistance Preload Afterload
Heart Rate
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Humoral
Adrenal medulla Catecholamines Hypothalamopituitary response Adrenocorticotropic hormone Vasopressin Renin-angiotensinaldosterone system
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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
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Stroke Volume
Preload (LVEDV) Reflects patients 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
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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
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Other Classifications
Hypovolemic or Hemorrhagic Cardiogenic Obstructive Distributive
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Cardiogenic
Hypovolemic Distributive Septic early late
No change
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Evaluation
Regardless of the cause: ABCs
First assess airway patency, ventilation, then circulatory system
Respiratory Performance
Respiratory rate and pattern, work of breathing, oxygenation (color), level of alertness
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Circulation
Heart rate, BP, perfusion, and pulses, liver size CVP monitoring may be helpful
Evaluation
Early Signs of Shock sinus tachycardia delayed capillary refill fussy, irritable Late Signs of Shock bradycardia altered mental status (lethargy, coma) hypotonia, decreased DTRs Cheyne-Stokes breathing hypotension is a very late sign Lower limit of SBP = 70 + (2 x age in years)
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Cardiovascular Assessment
Heart Rate
Too high: 180 bpm for infants, 160 bpm for children >1year old
Skin Perfusion
Capillary refill time Temperature Color Mottling
Blood Pressure
Lower limit of SBP = 70 + (2 x age in years)
CNS Perfusion
Recognition of parents Reaction to pain Muscle tone Pupil size
Peripheral Pulses
Present/Absent Strength (diminished, normal, bounding)
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Renal Perfusion
UOP >1cc/kg/hr
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
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Treatment
Circulation
Based on presumed etiology Rapid restoration of intravascular volume PIV-if unstable you have 60-90 seconds I.O. if less than 4-6 years old Central venous catheter Use isotonic fluid: NS, LR, or 5% albumin PRBCs to replace blood loss or if still unstable after 60cc/kg of crystalloid
anemia is poorly tolerated in the stressed, hypoxic, hemodynamically unstable patient
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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
2.5-15 mcg/kg/min: mostly beta-1, some beta-2 may be useful in cardiogenic shock
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Epinephrine
0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2 > 0.1 to 0.2 mcg/kg/min: alpha-1
Vasoactive/Cardiotonic Agents
Norepinephrine
0.05-0.2mcg/kg/min: only alpha and beta-1
Use up to 1mcg/kg/min
Milrinone
50mcg/kg load then 0.375-0.75mcg/kg/min: phosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effect on pulmonary vasculature)
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Phenylephrine
0.1-0.5mcg/kg/min: pure alpha
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
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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
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Treatment
Solution Na+ NS 154 LR 130 Plasmalyte 140 Cl154 109 98 K+ 0 4 5 Ca++ 0 3 0 Mg++ 0 0 3 Buffer None Lactate Acetate & Gluconate
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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
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
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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
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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
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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
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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
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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
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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
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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)
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Distributive Shock
Etiologies
Anaphylaxis Anaphylactoid reactions Spinal cord injury/spinal shock Head injury Early sepsis Drug intoxication
Barbiturates, Phenothiazines, Antihypertensives
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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
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Metabolic Issues
Electrolytes
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
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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
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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 LFTs, follow CNS and pulmonary status
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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
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Conclusion
Goal of therapy is identification, evaluation, and treatment of shock in its earliest stage Initial priorities are for the ABCs Fluid resuscitation begins with 20cc/kg of crystalloid or 10cc/kg of colloid Subsequent treatment depends on the etiology of shock and the patients hemodynamic condition Successful resuscitation depends on early and judicious intervention
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