SHOCK IN CHILDREN

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

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

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

Hemodynamics Textbook of Pediatric Advanced Life Support, 1988

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

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

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

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

Other Classifications Hypovolemic or Hemorrhagic Cardiogenic Obstructive Distributive

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

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

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)

Cardiovascular Assessment Heart Rate Too high: 180 bpm for infants, 160 bpm for children >1year old Blood Pressure Lower limit of SBP = 70 + (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

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

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 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

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 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) 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

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

Treatment Solution Na+ Cl- K+ Ca++ Mg++ Buffer NS 154 154 0 0 0 None LR 130 109 4 3 0 Lactate Plasmalyte 140 98 5 0 3 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

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

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

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

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

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

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

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

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)

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

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

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

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

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

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

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