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UTHSCSA

Pediatric Resident Curriculum for the PICU

SHOCK IN CHILDREN

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

Other Definitions
Blood Pressure
BP = CO x SVR

Cardiac Output
CO = SV X HR

Vascular Tone (SVR)


Regulated by several mechanisms

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

Hemodynamics
Myocardial Contractility Stroke Volume Cardiac Output Blood Pressure Systemic Vascular Resistance Preload Afterload

Heart Rate

UTHSCSA

Textbook of Pediatric Advanced Life Support, 1988

Pediatric Resident Curriculum for the PICU

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-angiotensinaldosterone system

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

Other Classifications
Hypovolemic or Hemorrhagic Cardiogenic Obstructive Distributive

UTHSCSA

Pediatric Resident Curriculum for the PICU

Cardiovascular Changes in Shock


Type Preload Afterload Contractility

Cardiogenic
Hypovolemic Distributive Septic early late

No change

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Circulation
Heart rate, BP, perfusion, and pulses, liver size CVP monitoring may be helpful

Pediatric Resident Curriculum for the PICU

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)

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Epinephrine
0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2 > 0.1 to 0.2 mcg/kg/min: alpha-1

Pediatric Resident Curriculum for the PICU

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)

UTHSCSA

Phenylephrine
0.1-0.5mcg/kg/min: pure alpha

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

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

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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)

UTHSCSA

Pediatric Resident Curriculum for the PICU

Distributive Shock

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

Pediatric Resident Curriculum for the PICU

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

UTHSCSA

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